Host–Candida auris interactions in the skin

Suppression of IL-17-mediated responses is critical for cutaneous antifungal defenses.

“It is likely that suppression of IL-17-mediated responses is critical for cutaneous antifungal defenses [3,55]”

• cites [3] X Huang, 2021, Murine model of colonization with fungal pathogen Candida auris to explore skin tropism, host risk factors and therapeutic strategies, Cell Host Microbe sourceDisputed

  The Results section reports that mice lacking IL-17R-dependent responses had significantly greater C. auris skin colonization. The Discussion likewise says a competent IL-17R pathway helps keep the fungus in check. Thus, the paper presents IL-17 responses—not their suppression—as protective for cutaneous antifungal defense. (LLM, conf=0.88)

  Checked by a reasoning model — may be wrong.

  Experimental — accuracy not yet measured
• cites [55] G Guggino, 2015, The in vitro addition of methotrexate and/or methylprednisolone determines peripheral reduction in Th17 and expansion of conventional Treg and of IL-10 producing Th17 lymphocytes in patients with early rheumatoid arthritis, Rheumatol Int sourceNot checked — no full text of the source

Diabetes has been repeatedly associated with an increased risk of C. auris systemic infection.

“diabetes has also been repeatedly associated with an increased risk of C. auris systemic infection [15,40–43].”

• cites [15] SR Lockhart, 2017, Simultaneous emergence of multidrug-resistant Candida auris on 3 continents confirmed by whole-genome sequencing and epidemiological analyses, Clin Infect Dis sourcePartly supported

  The Results (Case Patient Description; page not provided) identify diabetes as the most common underlying condition among 41 patients with C. auris infection. But this case description does not compare infection risk in people with and without diabetes, establish an increased risk of systemic infection, or show a repeated association. (LLM, conf=0.88)

  Experimental — accuracy not yet measured
• cites [40] Z Khan, 2018, Invasive Candida auris infections in Kuwait hospitals: epidemiology, antifungal treatment and outcome, Infection sourceNot checked — no full text of the source
• cites [41] KH Alanazi, 2025, An overview of healthcare-associated Candida auris outbreaks in Ministry of Health hospitals-Saudi Arabia 2020-2022; retrospective multicentric study, PLoS One sourceDisputed

  The Background lists diabetes as a risk factor for C. auris acquisition generally, but does not establish a repeated association with systemic infection. In the Results (Table 3; page unavailable), diabetes was significantly more common among colonized patients than infected patients—the opposite direction for the paper’s infection-versus-colonization comparison. (LLM, conf=0.86)

  Checked by a reasoning model — may be wrong.

  Experimental — accuracy not yet measured
• cites [42] A Munshi, 2024, Risk factors, antifungal susceptibility, complications, and outcome of Candida auris bloodstream infection in a tertiary care center in the western region of Saudi Arabia, J Infect Public Health sourceNot checked — no full text of the source
• cites [43] HA Amer, 2023, Characteristics and mitigation measures of Candida auris infection: descriptive analysis from a quaternary care hospital in Saudi Arabia, 2021-2022, J Epidemiol Glob Health sourcePartly supported

  The Discussion (page not supplied) says diabetes can suppress immune function and make patients vulnerable to fungal infections such as C. auris. The Results (page not supplied) report diabetes in 27.1% of cases, but the study does not establish an increased risk specifically of systemic infection or document a repeated association; 57% of its cases were colonized. (LLM, conf=0.84)

  Experimental — accuracy not yet measured

Cyclophosphamide-induced neutropenia increased mortality in mouse models of systemic C. auris infection.

“Cyclophosphamide-induced neutropenia increased mortality in mouse models of systemic C. auris infection [57,58]”

• cites [57] H Xin, 2019, Experimental mouse models of disseminated Candida auris infection, mSphere sourceDisputed

  The Results (Figs. 2 and 3; page unavailable) report no significant survival difference between cyclophosphamide-treated and untreated mice. Although the Discussion describes greater susceptibility and faster death in treated A/J mice, untreated A/J mice also reached 100% mortality; the paper does not establish the claimed increase in mortality. (LLM, conf=0.89)

  Checked by a reasoning model — may be wrong.

  Experimental — accuracy not yet measured
• cites [58] R Ben-Ami, 2017, Multidrug-resistant Candida haemulonii and C. auris, Tel Aviv, Israel, Emerg Infect Dis sourcePartly supported

  The Mouse Model of Disseminated Candidiasis methods say the mice received cyclophosphamide for immunosuppression, and the Results report rapid death after C. auris infection. The paper does not report a comparison with mice without cyclophosphamide or establish that neutropenia increased mortality. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: Findings from murine and ex vivo skin models of C. auris colonization and infection are relevant to human C. auris skin colonization and infection.

Unlike other Candida species, C. auris exhibits a distinct capacity for persistent skin colonization.

“Unlike other Candida species, C. auris exhibits a distinct capacity for persistent skin colonization.”

• cites [3] X Huang, 2021, Murine model of colonization with fungal pathogen Candida auris to explore skin tropism, host risk factors and therapeutic strategies, Cell Host Microbe sourceSupported
• cites [4] DM Proctor, 2023, One population, multiple lifestyles: commensalism and pathogenesis in the human mycobiome, Cell Host Microbe sourcePartly supported

  The Introduction’s “Persistent colonization of skin” section says C. auris can colonize patients’ skin for months or as long as a year. It also reports higher skin bioburden and denser ex vivo skin biofilms than other Candida species, but does not establish that persistent skin colonization itself distinguishes C. auris from other Candida species. (LLM, conf=0.82)

  Experimental — accuracy not yet measured
• cites [5] MS Lionakis, 2024, Candida auris Infections, N Engl J Med sourceNot checked — no full text of the source
• cites [6] DJ Santana, 2023, A Candida auris-specific adhesin, Scf1, governs surface association, colonization, and virulence, Science sourceSupported
• cites [7] KA Towns, 2024, Intradermal infection and dissemination of Candida auris in immunocompetent and immunocompromised mouse models, Microbiol Spectr sourceSupported

Treatment of C. auris is complicated by widespread resistance to approved antifungal drugs.

“Treatment is further complicated by widespread resistance to approved antifungal drugs [14,15].”

• cites [14] M Lyman, 2023, Worsening spread of Candida auris in the United States, 2019 to 2021, Ann Intern Med sourcePartly supported

  The Results (Drug Resistance; page not provided) report resistance to azoles in 86% of tested isolates and to amphotericin B in 26%, supporting concern about resistance to antifungal drugs. But the same section reports echinocandin resistance below 5%, and the Discussion says it remains uncommon despite echinocandins being first-line treatment. Thus, “widespread resistance” overstates the finding if applied to approved antifungals generally. (LLM, conf=0.85)

  Experimental — accuracy not yet measured
• cites [15] SR Lockhart, 2017, Simultaneous emergence of multidrug-resistant Candida auris on 3 continents confirmed by whole-genome sequencing and epidemiological analyses, Clin Infect Dis sourceSupported

The outer mannan layer of C. auris consists of two unique Mα1-phosphate side chains not found in other Candida species.

“The outer mannan layer of C. auris consists of two unique Mα1-phosphate side chains not found in other Candida species [18].”

• cites [18] M Bruno, 2020, Transcriptional and functional insights into the host immune response against the emerging fungal pathogen Candida auris, Nat Microbiol sourcePartly supported

  The Results section, “Unique structure of C. auris mannans” (page unavailable), identifies two distinct mannose-phosphate side chains as a unique feature of C. auris mannan. The paper compares C. auris with C. albicans, but does not establish that the side chains are absent from all other Candida species. (LLM, conf=0.84)

  Experimental — accuracy not yet measured

Healthcare isolates from the northeast, southeast, mountain, and west-coastal regions of the US are predominantly resistant to azoles.

“healthcare isolates from the northeast, southeast, mountain, and west-coastal regions of the US are predominantly resistant to azoles [14].”

• cites [14] M Lyman, 2023, Worsening spread of Candida auris in the United States, 2019 to 2021, Ann Intern Med sourceSupported

Diabetes is an underlying condition among patients with C. auris skin colonization, identified in 52% of cases.

“Surveillance studies across diverse geographical regions have identified diabetes as an underlying condition among patients with C. auris skin colonization (52% of cases) [37–39]”

• cites [37] SP Arenas, 2024, Persistent colonization of, Infect Control Hosp EpidemiolNot checked yet

  Not checked in the free run.

• cites [38] SA Alowais, 2025, Risk factors and outcomes for invasive infection among patients colonized with Candidozyma auris: a case-control study, Antibiotics (Basel) sourcePartly supported

  The Results (§2.1; page unavailable) identify diabetes mellitus among patients with C. auris colonization. They do not report that 52% of skin-colonized patients had diabetes; the study also included colonization detected at non-skin sites and was conducted at a single center, not across diverse regions. (LLM, conf=0.84)

  Experimental — accuracy not yet measured
• cites [39] KE Saunders, 2025, Risk factors associated with progression to clinical Candida auris infection among adults with previous colonization-Florida, 2019-2023, Clin Infect Dis sourcePartly supported

  The paper’s background passage identifies diabetes among previously reported medical risk factors for C. auris colonization or infection. It does not report diabetes in 52% of patients with skin colonization; the 52.4% figure in the Results refers to neurologic conditions among patients who progressed to clinical infection. (LLM, conf=0.87)

  Experimental — accuracy not yet measured

C. auris strains from the Mid-Atlantic regions are largely resistant to azoles and amphotericin B.

“C. auris strains from the Mid-Atlantic regions are largely resistant to azoles and amphotericin B.”

• cites [14] M Lyman, 2023, Worsening spread of Candida auris in the United States, 2019 to 2021, Ann Intern Med sourceSupported

Short-term exposure to a high-fat western diet did not increase skin colonization by C. auris in mice.

“short-term exposure to a high-fat western diet did not increase skin colonization by C. auris in mice [3].”

• cites [3] X Huang, 2021, Murine model of colonization with fungal pathogen Candida auris to explore skin tropism, host risk factors and therapeutic strategies, Cell Host Microbe sourcePartly supported

  The Methods (page unavailable) say mice received a high-fat or control diet for two weeks before colonization, and the Results (page unavailable) report no increase in C. auris skin colonization with the high-fat diet. The copy does not identify that diet as a specifically Western diet. (LLM, conf=0.83)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: Findings from murine and ex vivo skin models of C. auris colonization and infection are relevant to human C. auris skin colonization and infection.

Many hospital-grade disinfectants have limited efficacy against C. auris.

“Notably, many hospital-grade disinfectants have limited efficacy against C. auris [12,64,65].”

• cites [12] DM Proctor, 2021, Integrated genomic, epidemiologic investigation of Candida auris skin colonization in a skilled nursing facility, Nat Med sourceCould not verify

  The Abstract and Discussion address chlorhexidine (CHG) as a skin antiseptic and report persistent C. auris colonization despite CHG bathing. They do not assess whether many hospital-grade disinfectants have limited efficacy against C. auris; searches for disinfectants and environmental cleaning found no passage establishing that claim. (LLM, conf=0.72)

  Experimental — accuracy not yet measured
• cites [64] A Abdolrasouli, 2017, In vitro efficacy of disinfectants utilised for skin decolonisation and environmental decontamination during a hospital outbreak with Candida auris, Mycoses sourceNot checked — no full text of the source
• cites [65] RM Welsh, 2017, Survival, persistence, and isolation of the emerging multidrug-resistant pathogenic yeast Candida auris on a plastic health care surface, J Clin Microbiol sourceCould not verify

  The Discussion reports that C. auris persists on plastic surfaces for weeks and calls for effective cleaning and disinfection, but does not assess disinfectant efficacy. A search for hospital-grade disinfectants and their efficacy found no passage addressing whether many have limited efficacy against C. auris. (LLM, conf=0.76)

  Experimental — accuracy not yet measured

Immunosuppressive medications, especially corticosteroids, have been reported to be a predisposing factor for C. auris colonization.

“Immunosuppressive medications, especially corticosteroids, have been reported to be a predisposing factor for C. auris colonization.”

• cites [42] A Munshi, 2024, Risk factors, antifungal susceptibility, complications, and outcome of Candida auris bloodstream infection in a tertiary care center in the western region of Saudi Arabia, J Infect Public Health sourceNot checked — no full text of the source
• cites [54] M Katsiari, 2025, Impact of Candida auris on critically ill patients: a three-year observational study in a Greek intensive care unit, Pathogens sourcePartly supported

  The Discussion (page not available) lists corticosteroid use among potential risk factors in the case series, but frames the investigation around C. auris infection, not acquisition of colonization. The Results (§3.1, page not available) compare infected with colonized patients and find higher corticosteroid use in the infected group, a difference that was not statistically significant. The paper therefore does not establish immunosuppressive medications as a predisposing factor for colonization. (LLM, conf=0.83)

  Experimental — accuracy not yet measured

Vancomycin impairs lymphocyte-dependent IL-17 responses at mucosal barriers.

“and to impair lymphocyte-dependent IL-17 responses at mucosal barriers [49].”

• cites [49] RA Drummond, 2022, Long-term antibiotic exposure promotes mortality after systemic fungal infection by driving lymphocyte dysfunction and systemic escape of commensal bacteria, Cell Host Microbe sourceSupported

Topical application of C. auris in diabetic db/db mice did not increase skin colonization.

“a study using topical application of C. auris in diabetic db/db mice, a widely used genetic model of type 2 diabetes, did not increase skin colonization [3]”

• cites [3] X Huang, 2021, Murine model of colonization with fungal pathogen Candida auris to explore skin tropism, host risk factors and therapeutic strategies, Cell Host Microbe sourceSupported

• AssumptionRests on an assumption: Findings from murine and ex vivo skin models of C. auris colonization and infection are relevant to human C. auris skin colonization and infection.

Patients with long-term hospital stays, especially those in long-term acute care hospitals (LTACHs), were found to be likely to have C. auris skin colonization.

“As a result, patients with long-term hospital stays, especially those in long-term acute care hospitals (LTACHs) [66,67], were found to be likely to have C. auris skin colonization.”

• cites [66] J Rossow, 2021, Factors associated with Candida auris colonization and transmission in skilled nursing facilities with ventilator units, New York, 2016-2018, Clin Infect Dis sourcePartly supported

  The Results (page unavailable) associate a recent acute-care hospital visit with C. auris colonization among ventilator-skilled-nursing-facility residents, and the Discussion describes LTACH populations as high-yield for detection. The study used skin-site swabs, but it did not establish that longer hospital stays increased colonization risk or directly test that association in LTACH patients. (LLM, conf=0.87)

  Experimental — accuracy not yet measured
• cites [67] DW Eyre, 2018, A Candida auris outbreak and its control in an intensive care setting, N Engl J Med sourceNot checked — no full text of the source

The human skin mycobiome regulates C. auris colonization in the skin.

“A previous study shows that the human skin mycobiome regulates C. auris colonization in the skin [12].”

• cites [12] DM Proctor, 2021, Integrated genomic, epidemiologic investigation of Candida auris skin colonization in a skilled nursing facility, Nat Med sourcePartly supported

  The Results (Longitudinal analysis of C. auris colonization) found that Malassezia-diverse skin communities rarely transitioned to C. auris predominance. The Discussion interprets this as suggesting that commensal communities resist invasion, but the observational findings do not establish that the mycobiome regulates colonization. (LLM, conf=0.86)

  Experimental — accuracy not yet measured

Approximately 35% of patients who received corticosteroids were associated with C. auris colonization.

“Studies assessing potential risk factors of C. auris show that ~35% of patients who received corticosteroids were associated with C. auris colonization [42,54]”

• cites [42] A Munshi, 2024, Risk factors, antifungal susceptibility, complications, and outcome of Candida auris bloodstream infection in a tertiary care center in the western region of Saudi Arabia, J Infect Public Health sourceNot checked — no full text of the source
• cites [54] M Katsiari, 2025, Impact of Candida auris on critically ill patients: a three-year observational study in a Greek intensive care unit, Pathogens sourcePartly supported

  Results §3.1 reports that 34.6% of colonized patients were receiving corticosteroids, compared with 83.3% of infected patients; the difference was not statistically significant (p = 0.064). The claim reverses the denominator: the paper does not say that approximately 35% of patients receiving corticosteroids were colonized. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

C. auris strains belonging to clade III highly express SCF1 and ALS4112, associated with greater adherence capacity.

“C. auris strains belonging to clade III highly express SCF1 and ALS4112, associated with greater adherence capacity.”

• cites [6] DJ Santana, 2023, A Candida auris-specific adhesin, Scf1, governs surface association, colonization, and virulence, Science sourcePartly supported

  In “C. auris relies on SCF1 for adhesive plasticity” (page unavailable), SCF1 transcript abundance is positively correlated with adhesion across isolates, but the paper says this variation occurs regardless of clade—not specifically in clade III. In “Polymer surface attachment by the adhesin SCF1” (page unavailable), ALS4112 overexpression is associated with flocculation and aggregation, not greater surface adherence. The copy therefore does not support the claimed high expression of both genes in clade III. (LLM, conf=0.88)

  Experimental — accuracy not yet measured
• cites [11] G Zhao, 2025, Adhesin Als4112 promotes Candida auris skin colonization through interactions with keratinocytes and extracellular matrix proteins, Nat Commun sourcePartly supported

  The Results section, “Modulating ALS4112 expression levels regulates C. auris adherence to keratinocytes” (page unavailable), reports that ALS4112 expression correlates with keratinocyte adherence across isolates, regardless of clade. The Results section, “Als4112 is the major adhesin mediating keratinocyte adherence” (page unavailable), identifies one highly adherent Clade III strain, but does not establish that Clade III strains generally highly express ALS4112 or SCF1. The Discussion (page unavailable) says SCF1 deletion did not reduce adherence in the keratinocyte assay; the claimed joint expression pattern is therefore not supported. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

SCF1 functions redundantly with the adhesin IFF4109, as their double deletion in the Δscf1 Δiff4109 mutant strain significantly decreased skin colonization.

“SCF1 functions redundantly with the adhesin IFF4109, a member of the IFF/HYR adhesin family, as their double deletion in the Δscf1 Δiff4109 mutant strain significantly decreased skin colonization.”

• cites [6] DJ Santana, 2023, A Candida auris-specific adhesin, Scf1, governs surface association, colonization, and virulence, Science sourceSupported

• AssumptionRests on an assumption: Findings from murine and ex vivo skin models of C. auris colonization and infection are relevant to human C. auris skin colonization and infection.

Skin samples enriched for Malassezia species, including M. globosa, M. furfur, M. restricta, and M. arunalokei, which dominate the healthy human skin mycobiome, were rarely positive for C. auris.

“Skin samples enriched for Malassezia species, including M. globosa, M. furfur, M. restricta, and M. arunalokei, which dominate the healthy human skin mycobiome, were rarely positive for C. auris [12,69].”

• cites [12] DM Proctor, 2021, Integrated genomic, epidemiologic investigation of Candida auris skin colonization in a skilled nursing facility, Nat Med sourcePartly supported

  The Results section on longitudinal colonization identifies a community dominated by the four named Malassezia species as resembling healthy skin, and reports that this community rarely transitioned to C. auris predominance. It does not establish that Malassezia-enriched samples were rarely positive for C. auris; positivity and predominance are different measures. Page numbers are unavailable in our copy. (LLM, conf=0.83)

  Experimental — accuracy not yet measured
• cites [69] K Findley, 2013, Topographic diversity of fungal and bacterial communities in human skin, Nature sourcePartly supported

  The Human Skin Fungal Diversity section reports that Malassezia predominated at eleven skin sites in healthy volunteers, with M. restricta and M. globosa predominant at particular sites. It does not establish that all four named species dominate healthy skin; its species list does not include M. arunalokei. The paper also does not report whether Malassezia-enriched samples were positive for C. auris. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

The skin colonization potential varies among the different geographically stratified clades of C. auris.

“The skin colonization potential varies among the different geographically stratified clades of C. auris [3].”

• cites [3] X Huang, 2021, Murine model of colonization with fungal pathogen Candida auris to explore skin tropism, host risk factors and therapeutic strategies, Cell Host Microbe sourceSupported

• AssumptionRests on an assumption: Findings from murine and ex vivo skin models of C. auris colonization and infection are relevant to human C. auris skin colonization and infection.

Deletion of Δscf1Δiff4109 and ΔAls4112 significantly reduced skin colonization.

“Moreover, deletion of Δscf1Δiff4109 and ΔAls4112 significantly reduced skin colonization, suggesting a vital role of these adhesins in C. auris colonization of the skin [6,11].”

• cites [6] DJ Santana, 2023, A Candida auris-specific adhesin, Scf1, governs surface association, colonization, and virulence, Science sourcePartly supported

  In “SCF1 promotes long-term colonization and virulence” (page not available), the paper reports that loss of SCF1 and IFF4109 diminished colonization of human skin explants and murine skin. It does not report that deletion of ALS4112 reduced skin colonization; its discussion of ALS4112 concerns flocculation and aggregation. (LLM, conf=0.88)

  Experimental — accuracy not yet measured
• cites [11] G Zhao, 2025, Adhesin Als4112 promotes Candida auris skin colonization through interactions with keratinocytes and extracellular matrix proteins, Nat Commun sourceSupported

• AssumptionRests on an assumption: Findings from murine and ex vivo skin models of C. auris colonization and infection are relevant to human C. auris skin colonization and infection.

Clinical isolates of C. auris exhibiting aggregative phenotypes often harbor amplification of the sub-telomeric ALS4112 locus, conferring robust biofilm formation and colonization on murine skin.

“Clinical isolates of C. auris exhibiting aggregative phenotypes often harbor amplification of the sub-telomeric ALS4112 locus, conferring robust biofilm formation and colonization on murine skin [73].”

• cites [73] J Bing, 2023, Clinical isolates of Candida auris with enhanced adherence and biofilm formation due to genomic amplification of ALS4, PLoS Pathog sourcePartly supported

  The Results sections on ALS4 genomic analysis and newborn-mouse skin colonization report that amplified ALS4 contributes to a new aggregative phenotype and that strain SJ02 formed robust biofilms and colonized mouse skin. The claim overgeneralizes this to aggregative isolates ‘often’ harboring amplification: the paper distinguishes another aggregative phenotype, and its surveyed isolates rarely had more than two ALS4 copies. The locus is named ALS4 (also B9J08_004112), not ALS4112; murine skin colonization was demonstrated for SJ02, not for aggregative isolates generally (pages unavailable in our copy). (LLM, conf=0.88)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: Findings from murine and ex vivo skin models of C. auris colonization and infection are relevant to human C. auris skin colonization and infection.

Patients colonized with C. auris on their skin harbor a distinct skin bacterial microbiome compared with uncolonized individuals from the same facility.

“A point prevalence survey conducted by Proctor and colleagues in a ventilator-capable skilled nursing facility in Chicago showed that patients colonized with C. auris on their skin harbor a distinct skin bacterial microbiome compared with uncolonized individuals from the same facility [12].”

• cites [12] DM Proctor, 2021, Integrated genomic, epidemiologic investigation of Candida auris skin colonization in a skilled nursing facility, Nat Med sourcePartly supported

  The Results section, “Underlying microbiome associated with C. auris colonization” (page unavailable), reports that bacterial species distinguished C. auris culture-positive skin samples from culture-negative samples in the skilled nursing facility. That supports a difference in skin bacterial microbiomes, but the analysis compares samples, not specifically colonized patients with uncolonized individuals. (LLM, conf=0.84)

  Experimental — accuracy not yet measured

A HOG1-deficient mutant strain exhibited reduced epidermal colonization, intradermal persistence, and dissemination to distant organs following epicutaneous and intradermal infections in mice.

“A HOG1-deficient mutant strain exhibited reduced epidermal colonization, intradermal persistence, and dissemination to distant organs following epicutaneous and intradermal infections in mice [76].”

• cites [76] R Shivarathri, 2024, The Candida auris Hog1 MAP kinase is essential for the colonization of murine skin and intradermal persistence, mBio sourcePartly supported

  The Results section reports reduced skin fungal burden after epicutaneous and intradermal infection with the hog1Δ mutant, supporting reduced epidermal colonization and intradermal persistence. It also reports reduced kidney and brain burdens, but Fig. 5E specifies that these were measured after a separate systemic infection, not as dissemination following the skin infections. (LLM, conf=0.90)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: Findings from murine and ex vivo skin models of C. auris colonization and infection are relevant to human C. auris skin colonization and infection.

Adhesins Scf1, Iff4109, and Als4112 play a vital role in C. auris colonization of the skin.

“suggesting a vital role of these adhesins in C. auris colonization of the skin [6,11].”

• cites [6] DJ Santana, 2023, A Candida auris-specific adhesin, Scf1, governs surface association, colonization, and virulence, Science sourcePartly supported

  In “SCF1 promotes long-term colonization and virulence” (page unavailable), the paper reports that loss of SCF1 and IFF4109 diminished C. auris colonization of human skin explants and murine skin. It does not establish a skin-colonization role for ALS4112; the “Polymer surface attachment” section instead associates ALS4112 overexpression with flocculation and aggregation. (LLM, conf=0.90)

  Experimental — accuracy not yet measured
• cites [11] G Zhao, 2025, Adhesin Als4112 promotes Candida auris skin colonization through interactions with keratinocytes and extracellular matrix proteins, Nat Commun sourceSupported

• AssumptionRests on an assumption: Findings from murine and ex vivo skin models of C. auris colonization and infection are relevant to human C. auris skin colonization and infection.

The protein kinase Hog1 governs C. auris adaptation to host-imposed stress conditions.

“The protein kinase Hog1 governs C. auris adaptation to host-imposed stress conditions [75,76].”

• cites [75] AM Day, 2018, Hog1 regulates stress tolerance and virulence in the emerging fungal pathogen Candida auris, mSphere sourceSupported
• cites [76] R Shivarathri, 2024, The Candida auris Hog1 MAP kinase is essential for the colonization of murine skin and intradermal persistence, mBio sourceSupported

C. auris-positive dog ears exhibited reduced abundance of Malassezia species.

“Similarly, C. auris-positive dog ears exhibited reduced abundance of Malassezia species [70].”

• cites [70] A Yadav, 2023, J Fungi (Basel) sourcePartly supported

  The Results (page unavailable) report a seeming negative correlation between C. auris and Malassezia ITS-read abundance among three C. auris-positive dogs. That supports a possible association, but the paper does not establish that C. auris-positive dog ears generally had reduced Malassezia abundance compared with negative ears; it also reports wide variation among C. auris-negative dogs. (LLM, conf=0.84)

  Experimental — accuracy not yet measured

C. auris abundance correlated with other Candida species such as C. tropicalis, C. parapsilosis, C. orthopsilosis, and C. metapsilosis.

“Conversely, C. auris abundance correlated with other Candida species such as C. tropicalis, C. parapsilosis, C. orthopsilosis, and C. metapsilosis (Fig 2) [12].”

• cites [12] DM Proctor, 2021, Integrated genomic, epidemiologic investigation of Candida auris skin colonization in a skilled nursing facility, Nat Med sourcePartly supported

  The Results section on longitudinal colonization (page unavailable) places C. auris in the same fungal community type as all four named Candida species. It does not report that C. auris abundance correlated with their abundances; co-occurrence does not establish that relationship. (LLM, conf=0.84)

  Experimental — accuracy not yet measured

Patients who were not colonized with C. auris harbored a distinct set of bacteria, such as Staphylococcus hominis, Staphylococcus caprae, Anaerococcus nagyae, Peptoniphilus tyrrelliae, Anaerococcus octavius, Corynebacterium tuberculostearicum, and Staphylococcus epidermidis.

“In contrast, patients who were not colonized with C. auris harbored a distinct set of bacteria, such as Staphylococcus hominis, Staphylococcus caprae, Anaerococcus nagyae, Peptoniphilus tyrrelliae, Anaerococcus octavius, Corynebacterium tuberculostearicum, and Staphylococcus epidermidis (Fig 2) [12].”

• cites [12] DM Proctor, 2021, Integrated genomic, epidemiologic investigation of Candida auris skin colonization in a skilled nursing facility, Nat Med sourcePartly supported

  The Results section, “Underlying microbiome associated with C. auris colonization” (page not provided), associates Staphylococcus hominis, S. caprae, Corynebacterium tuberculostearicum, and S. epidermidis with C. auris culture-negative samples. Our copy does not identify Anaerococcus nagyae, Peptoniphilus tyrrelliae, or Anaerococcus octavius as part of that group. The analysis also compares samples, rather than establishing that every patient described as noncolonized harbored these bacteria. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

Hog1 confers resistance to osmotic, cationic, acid, and reactive oxygen species-induced stress.

“Specifically, Hog1 confers resistance to osmotic, cationic, acid, and reactive oxygen species-induced stress [75,76].”

• cites [75] AM Day, 2018, Hog1 regulates stress tolerance and virulence in the emerging fungal pathogen Candida auris, mSphere sourcePartly supported

  The Results section ('Hog1-mediated stress resistance in C. auris') reports that cells lacking Hog1 were sensitive to osmotic and cationic stress, H2O2, and highly acidic conditions. The claim omits important limits: Hog1 was dispensable in moderately acidic conditions and for resistance to the organic oxidative stress-inducing agent tert-butyl hydroperoxide, so the findings do not establish resistance to acid or reactive oxygen species-induced stress generally. (LLM, conf=0.86)

  Experimental — accuracy not yet measured
• cites [76] R Shivarathri, 2024, The Candida auris Hog1 MAP kinase is essential for the colonization of murine skin and intradermal persistence, mBio sourcePartly supported

  The Introduction says Hog1 regulates adaptation to high osmolarity and oxidative stress in C. albicans and describes its broader role in fungal stress tolerance. The Results also link C. auris Hog1 to survival during ROS-associated phagocytic killing. Our copy does not establish resistance to cationic or acid stress, so it supports only part of the attributed list. (LLM, conf=0.86)

  Experimental — accuracy not yet measured

Proctor and colleagues identified four distinct mycobiome clusters in patients, distinguished by the relative abundance of Malassezia and Candida species.

“Proctor and colleagues identified four distinct mycobiome clusters in patients, distinguished by the relative abundance of Malassezia and Candida species [12].”

• cites [12] DM Proctor, 2021, Integrated genomic, epidemiologic investigation of Candida auris skin colonization in a skilled nursing facility, Nat Med sourceSupported

Patients with C. auris skin colonization were frequently co-colonized with multidrug-resistant gram-negative bacteria, including Proteus mirabilis, Pseudomonas aeruginosa, Klebsiella pneumoniae, Providencia stuartii, and Morganella morganii.

“Patients with C. auris skin colonization were frequently co-colonized with multidrug-resistant gram-negative bacteria, including Proteus mirabilis, Pseudomonas aeruginosa, Klebsiella pneumoniae, Providencia stuartii, and Morganella morganii (Fig 2) [12,13].”

• cites [12] DM Proctor, 2021, Integrated genomic, epidemiologic investigation of Candida auris skin colonization in a skilled nursing facility, Nat Med sourcePartly supported

  The Results section (‘Underlying microbiome associated with C. auris colonization’; page unavailable) identifies four of the five named Gram-negative species as enriched in C. auris-positive samples. The copy does not establish that those bacteria were multidrug-resistant, and its mention of Morganella morganii in Extended Data Fig. 5 concerns an association with chlorhexidine concentration, not C. auris co-colonization. (LLM, conf=0.88)

  Experimental — accuracy not yet measured
• cites [13] DM Proctor, 2025, Clonal Candida auris and ESKAPE pathogens on the skin of residents of nursing homes, Nature sourceNot checked — no full text of the source

During systemic murine infection, fungal proliferation in the kidney and brain was significantly decreased in the Δhog1 mutant strain.

“Similarly, during systemic murine infection, fungal proliferation in the kidney and brain was significantly decreased in the Δhog1 mutant strain [76].”

• cites [76] R Shivarathri, 2024, The Candida auris Hog1 MAP kinase is essential for the colonization of murine skin and intradermal persistence, mBio sourceSupported

• AssumptionRests on an assumption: Findings from murine and ex vivo skin models of C. auris colonization and infection are relevant to human C. auris skin colonization and infection.

ALS4112 mediates keratinocyte adherence.

“A recent study performed unbiased insertional mutant screening in C. auris and confirmed that ALS4112 mediates keratinocyte adherence [11].”

• cites [11] G Zhao, 2025, Adhesin Als4112 promotes Candida auris skin colonization through interactions with keratinocytes and extracellular matrix proteins, Nat Commun sourceSupported

Inoculation of C. auris pmr1Δ and van1Δ mutant strains into the zebrafish model of invasive candidiasis results in increased neutrophil recruitment associated with reduced fungal burden.

“These mutant strains exhibited improved recognition and killing by human neutrophils ex vivo, and their inoculation into the zebrafish model of invasive candidiasis resulted in increased neutrophil recruitment, associated with reduced fungal burden [87].”

• cites [87] MV Horton, 2021, Candida auris cell wall mannosylation contributes to neutrophil evasion through pathways divergent from Candida albicans and Candida glabrata, mSphere sourceSupported

Hyperactivation of the Ras/cAMP/PKA pathway by BCY1 or PDE2 deletion attenuated the virulence during murine systemic infection by reducing the ability to thrive in nutrient-deficient conditions.

“Furthermore, hyperactivation of the Ras/cAMP/PKA pathway by BCY1 or PDE2 deletion attenuated the virulence during murine systemic infection by reducing the ability to thrive in nutrient-deficient conditions [79,80].”

• cites [79] J-S Kim, 2023, Deciphering the regulatory mechanisms of the cAMP/protein kinase A pathway and their roles in the pathogenicity of Candida auris, Microbiol Spectr sourcePartly supported

  The Results sections report reduced virulence in mice after PDE2 deletion and reduced survival under nutrient-starved conditions after BCY1 or PDE2 deletion; the paper also reports attenuated virulence after BCY1 deletion. But the Discussion says impaired survival under nutrient starvation *may* reduce virulence and identifies other potentially relevant effects. It does not establish nutrient-starvation sensitivity as the cause of the reduced virulence. (LLM, conf=0.88)

  Experimental — accuracy not yet measured
• cites [80] H Cha, 2025, Signaling pathways governing the pathobiological features and antifungal drug resistance of Candida auris, mBio sourcePartly supported

  The section on host temperature adaptation and thermotolerance (page unavailable) says that BCY1 or PDE2 deletion hyperactivates cAMP/PKA signaling, attenuates systemic virulence, and causes severe growth defects under nutrient-starved conditions within the host. It says those defects *may* lead to reduced virulence; the claim presents that proposed explanation as an established cause. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: Findings from murine and ex vivo skin models of C. auris colonization and infection are relevant to human C. auris skin colonization and infection.

In an epicutaneous model, both Rag2-deficient mice and Rag2 Il2rg double-knockout mice are highly susceptible to C. auris skin colonization.

“Similarly, Huang and colleagues demonstrated in an epicutaneous model that both Rag2-deficient mice, which lack T cells but retain ILC populations, as well as Rag2 Il2rg double-knockout mice, which lack ILCs in addition to all other lymphoid cells, were highly susceptible to C. auris skin colonization [3].”

• cites [3] X Huang, 2021, Murine model of colonization with fungal pathogen Candida auris to explore skin tropism, host risk factors and therapeutic strategies, Cell Host Microbe sourceSupported

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

During C. auris skin infection, macrophages appear to facilitate, rather than restrict, fungal persistence.

“Macrophages are pivotal in host defense against several fungal pathogens, yet during C. auris skin infection appears to facilitate, rather than restrict, fungal persistence [81].”

• cites [81] MS Lionakis, 2023, Immune responses to human fungal pathogens and therapeutic prospects, Nat Rev Immunol sourceCould not verify

  The Introduction (page unavailable) describes long-term C. auris skin colonization and identifies IL-17A and IL-17F as protective, but does not say whether macrophages facilitate persistence. The Invasive candidiasis section discusses macrophages in other Candida infections; searches for macrophage involvement in C. auris skin colonization found no passage addressing the claim. (LLM, conf=0.75)

  Experimental — accuracy not yet measured

Disruption of mitochondria and iron homeostasis restricts the proliferation of C. auris within macrophages.

“Disruption of mitochondria and iron homeostasis restricts the proliferation of C. auris within macrophages, underscoring the metabolic dependence of this phenomenon [91].”

• cites [91] C Simm, 2022, Disruption of iron homeostasis and mitochondrial metabolism are promising targets to inhibit Candida auris, Microbiol Spectr sourceSupported

In an intradermal mouse model, neutrophil accumulation is significantly lower in C. auris-infected compared to C. albicans-infected mice in vivo.

“Similarly, in an intradermal mouse model of C. auris infection, neutrophil accumulation was significantly lower in C. auris-infected compared to C. albicans-infected mice in vivo [85].”

• cites [85] A Datta, 2023, Differential skin immune responses in mice intradermally infected with Candida auris and Candida albicans, Microbiol Spectr sourceSupported

C. auris exhibits remarkable resistance to neutrophil phagocytosis and killing ex vivo, unlike C. albicans, attributable to its unique cell wall composition.

“Unlike C. albicans, C. auris exhibits remarkable resistance to neutrophil phagocytosis and killing ex vivo, attributable to its unique cell wall composition [18,84].”

• cites [18] M Bruno, 2020, Transcriptional and functional insights into the host immune response against the emerging fungal pathogen Candida auris, Nat Microbiol sourcePartly supported

  The Discussion (page unavailable) reports that a recent study found human neutrophils less able to kill C. auris than C. albicans. It does not establish resistance to neutrophil phagocytosis or attribute the reduced killing to cell-wall composition. The Results examine phagocytosis by macrophages, not neutrophils. (LLM, conf=0.86)

  Experimental — accuracy not yet measured
• cites [84] CJ Johnson, 2018, Emerging fungal pathogen Candida auris evades neutrophil attack, mBio sourcePartly supported

  The Observation section reports that human neutrophils engaged and killed C. auris far less effectively than C. albicans in coculture, supporting the ex vivo comparison. It does not establish that C. auris’s cell wall composition causes this resistance; searches for cell-wall composition and recognition found no such explanation in our copy. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

Flow cytometric and scRNA-seq analyses reveal increased accumulation of macrophages at the site of C. auris skin infection in mice.

“Flow cytometric and scRNA-seq analyses revealed increased accumulation of macrophages at the site of C. auris skin infection in mice [86], but their functional role remained poorly defined.”

• cites [86] A Balakumar, 2024, Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris, PLoS Pathog sourceSupported

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

IL-1Ra neutralization in C. auris-infected mice in vivo significantly reduces cutaneous fungal burden.

“Exogenous IL-1Ra decreased the killing capacity of neutrophils ex vivo against C. auris, while IL-1Ra neutralization in C. auris-infected mice in vivo significantly reduced cutaneous fungal burden, demonstrating that excessive IL-1Ra dampens protective neutrophil responses and favors fungal growth in the skin.”

• cites [86] A Balakumar, 2024, Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris, PLoS Pathog sourceSupported

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

scRNA-seq of C. auris murine skin during infection identifies IL1RN as a key host factor modulating neutrophil activity.

“scRNA-seq of C. auris murine skin during infection identified IL1RN (encoding IL-1 receptor antagonist, IL-1Ra) as a key host factor modulating neutrophil activity during C. auris infection [86].”

• cites [86] A Balakumar, 2024, Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris, PLoS Pathog sourceSupported

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

Deletion of FOX2 (β-oxidation), CAT2 (fatty acid transport), and ICL1 (glyoxylate cycle) results in defective growth in sweat media.

“Recent evidence suggests that deletion of FOX2 (β-oxidation), CAT2 (fatty acid transport), and ICL1 (glyoxylate cycle) results in defective growth in sweat media [77].”

• cites [77] JP Nicklas, 2025, Candida auris metabolism and growth preferences in physiologically relevant skin-like conditions, bioRxiv sourcePartly supported

  The Growth analysis section reports significantly reduced growth of FOX2, CAT2, and ICL1 deletion mutants in Sweat + 0.1% Sebum liquid medium, not sweat medium alone. It also describes CAT2 as assisting acetyl-CoA transport and breakdown, rather than fatty-acid transport. Page numbers were not provided in our copy. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

In an intradermal mouse model, IL-17+ ILCs accumulate in the skin during C. auris infection.

“In an intradermal mouse model, IL-17+ ILCs accumulated in the skin during C. auris infection [85].”

• cites [85] A Datta, 2023, Differential skin immune responses in mice intradermally infected with Candida auris and Candida albicans, Microbiol Spectr sourcePartly supported

  The Results section (page not provided) reports increased IL-17F+ ILCs in C. auris-infected skin versus PBS-injected skin at day 3, supporting accumulation of that subset. It does not report a corresponding increase in IL-17A+ ILCs; at day 14, both IL-17A+ and IL-17F+ ILCs accumulated less than in C. albicans-infected skin. The claim omits these subtype, timing, and comparator qualifications. (LLM, conf=0.85)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

In a zebrafish model of invasive candidiasis, neutrophil recruitment in vivo is reduced during C. auris compared to C. albicans infection.

“Using a zebrafish model of invasive candidiasis, reduced neutrophil recruitment in vivo was observed during C. auris compared to C. albicans infection [84].”

• cites [84] CJ Johnson, 2018, Emerging fungal pathogen Candida auris evades neutrophil attack, mBio sourceSupported

ILCs contribute to effective host defense against mucocutaneous fungal challenge.

“ILCs contribute to effective host defense against mucocutaneous fungal challenge [92,93].”

• cites [92] A Gladiator, 2013, Innate lymphoid cells: new players in IL-17-mediated antifungal immunity, PLoS Pathog sourcePartly supported

  The section “Which Cellular Sources Provide IL-17 during Fungal Infection?” reports that depleting ILC3s makes mice highly susceptible to oropharyngeal candidiasis, supporting a role in mucosal fungal defense. It does not establish the same protective role for ILCs across cutaneous infections or in humans; the paper says the human role remains a question. (LLM, conf=0.83)

  Experimental — accuracy not yet measured
• cites [93] I Beccacece, 2025, Cutaneous innate lymphoid populations drive IL-17A-mediated immunity in Nannizzia gypsea dermatophytosis, J Invest Dermatol sourceSupported

In ex vivo murine skin, the Δcna1 strain had significantly lower adhesion to the skin shortly post-association.

“In ex vivo murine skin, the Δcna1 strain had significantly lower adhesion to the skin shortly post-association [78].”

• cites [78] H Cha, 2025, The calcineurin pathway regulates extreme thermotolerance, cell membrane and wall integrity, antifungal resistance, and virulence in Candida auris, PLoS Pathog sourceSupported

• AssumptionRests on an assumption: Findings from murine and ex vivo skin models of C. auris colonization and infection are relevant to human C. auris skin colonization and infection.

C. auris neutrophil evasion is linked to its cell wall mannosylation.

“Recent work linked this neutrophil evasion to C. auris cell wall mannosylation [87].”

• cites [87] MV Horton, 2021, Candida auris cell wall mannosylation contributes to neutrophil evasion through pathways divergent from Candida albicans and Candida glabrata, mSphere sourceSupported

Exogenous IL-1Ra decreases the killing capacity of neutrophils ex vivo against C. auris.

“Exogenous IL-1Ra decreased the killing capacity of neutrophils ex vivo against C. auris, while IL-1Ra neutralization in C. auris-infected mice in vivo significantly reduced cutaneous fungal burden, demonstrating that excessive IL-1Ra dampens protective neutrophil responses and favors fungal growth in the skin.”

• cites [86] A Balakumar, 2024, Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris, PLoS Pathog sourceSupported

• AssumptionRests on an assumption: Findings from ex vivo human neutrophils and mouse models can be combined to infer mechanisms of human skin immunity.

C. auris can replicate within macrophages, using metabolic plasticity to survive and escape the phagolysosomal environment.

“Recent studies showed that C. auris can replicate within macrophages, using metabolic plasticity to survive and escape the phagolysosomal environment [90,91].”

• cites [90] H Weerasinghe, 2023, Candida auris uses metabolic strategies to escape and kill macrophages while avoiding robust activation of the NLRP3 inflammasome response, Cell Rep sourceNot checked — no full text of the source
• cites [91] C Simm, 2022, Disruption of iron homeostasis and mitochondrial metabolism are promising targets to inhibit Candida auris, Microbiol Spectr sourcePartly supported

  The Results report that C. auris replicated inside mouse bone marrow-derived macrophages, and the Discussion says metabolic flexibility is needed in glucose-poor host niches such as the macrophage phagosome (page numbers unavailable). The paper does not establish that metabolic plasticity enables C. auris to escape the phagolysosomal environment. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

The mannan-IL-1Ra axis represents a critical checkpoint exploited by C. auris to persist in the skin.

“This mannan-IL-1Ra axis represents a critical checkpoint exploited by C. auris to persist in the skin and a potential therapeutic target.”

• cites [86] A Balakumar, 2024, Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris, PLoS Pathog sourceSupported
• cites [87] MV Horton, 2021, Candida auris cell wall mannosylation contributes to neutrophil evasion through pathways divergent from Candida albicans and Candida glabrata, mSphere sourcePartly supported

  The Discussion (page not provided) says C. auris mannosylation protects it from neutrophil phagocytosis, supporting an immune-evasion role for mannan. The paper does not establish an IL-1Ra pathway or show that this mechanism enables persistence in skin; searches for IL-1Ra and skin persistence found no supporting passage. (LLM, conf=0.85)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

C. auris pmr1Δ and van1Δ mutant strains exhibit improved recognition and killing by human neutrophils ex vivo.

“These mutant strains exhibited improved recognition and killing by human neutrophils ex vivo, and their inoculation into the zebrafish model of invasive candidiasis resulted in increased neutrophil recruitment, associated with reduced fungal burden [87].”

• cites [87] MV Horton, 2021, Candida auris cell wall mannosylation contributes to neutrophil evasion through pathways divergent from Candida albicans and Candida glabrata, mSphere sourceSupported

In nutrient-poor environments lacking glucose, C. auris utilizes free fatty acids via β-oxidation, followed by the glyoxylate cycle to obtain energy from the carbon source.

“In nutrient-poor environments lacking glucose, C. auris utilizes free fatty acids via β-oxidation, followed by the glyoxylate cycle to obtain energy from the carbon source.”

• cites [77] JP Nicklas, 2025, Candida auris metabolism and growth preferences in physiologically relevant skin-like conditions, bioRxiv sourceSupported

CRISPR-mediated deletion of PMR1 and VAN1 in C. auris significantly reduces cell wall mannan content and reciprocally increases exposure of β-glucan and chitin.

“CRISPR-mediated deletion of PMR1 and VAN1, genes required for N-mannan synthesis and branching, significantly reduced cell wall mannan content and reciprocally increased exposure of β-glucan and chitin [87].”

• cites [87] MV Horton, 2021, Candida auris cell wall mannosylation contributes to neutrophil evasion through pathways divergent from Candida albicans and Candida glabrata, mSphere sourcePartly supported

  The Results sections on cell-wall structure and pathogen-associated molecular patterns report less mannan in the C. auris pmr1Δ and van1Δ mutants and greater surface exposure of β-glucan and chitin (pages unavailable). However, Materials and Methods explicitly says the mutants were generated by fusion PCR-based gene disruption without CRISPR-Cas9, so the claim's description of the deletion method is incorrect. (LLM, conf=0.95)

  Experimental — accuracy not yet measured

Ablation of the calcineurin pathway by CNA1 deletion in C. auris significantly reduced abscess and fungal burden in the murine skin in a subcutaneous infection model.

“Cha and colleagues demonstrated that ablation of the calcineurin pathway by CNA1 deletion in C. auris significantly reduced abscess and fungal burden in the murine skin in a subcutaneous infection model [78].”

• cites [78] H Cha, 2025, The calcineurin pathway regulates extreme thermotolerance, cell membrane and wall integrity, antifungal resistance, and virulence in Candida auris, PLoS Pathog sourceSupported

• AssumptionRests on an assumption: Findings from murine and ex vivo skin models of C. auris colonization and infection are relevant to human C. auris skin colonization and infection.

C. auris regulates other stress resistance pathways, such as calcineurin and Ras/cAMP/PKA pathways for thermotolerance, morphological plasticity, and biofilm formation, which contribute to pathogenesis in C. auris.

“C. auris further regulates other stress resistance pathways, such as calcineurin [78] and Ras/cAMP/PKA [79] pathways for thermotolerance, morphological plasticity, and biofilm formation, which contribute to pathogenesis in C. auris.”

• cites [78] H Cha, 2025, The calcineurin pathway regulates extreme thermotolerance, cell membrane and wall integrity, antifungal resistance, and virulence in Candida auris, PLoS Pathog sourcePartly supported

  The Discussion (page not provided) supports a role for calcineurin in extreme thermotolerance and pathogenicity in C. auris. But the Results section explicitly finds that calcineurin does not regulate pseudohyphal formation or biofilm formation, contrary to those parts of the claim. The separate Ras/cAMP/PKA citation is not assessed here. (LLM, conf=0.90)

  Experimental — accuracy not yet measured
• cites [79] J-S Kim, 2023, Deciphering the regulatory mechanisms of the cAMP/protein kinase A pathway and their roles in the pathogenicity of Candida auris, Microbiol Spectr sourceSupported

CNA1 is indispensable for virulence properties needed for C. auris skin colonization and infection.

“This suggests that the CNA1 is indispensable for virulence properties needed for C. auris skin colonization and infection [78].”

• cites [78] H Cha, 2025, The calcineurin pathway regulates extreme thermotolerance, cell membrane and wall integrity, antifungal resistance, and virulence in Candida auris, PLoS Pathog sourceSupported

• AssumptionRests on an assumption: Findings from murine and ex vivo skin models of C. auris colonization and infection are relevant to human C. auris skin colonization and infection.

Cells lacking ACE2 fail to separate following budding and remain clumped together or "aggregate", becoming resistant to physical stress and disruption.

“As such, cells lacking ACE2 fail to separate following budding and remain clumped together or “aggregate”, becoming resistant to physical stress and disruption [111].”

• cites [111] AM Borman, 2016, Comparative pathogenicity of United Kingdom isolates of the emerging pathogen Candida auris and other key pathogenic Candida species, mSphere sourcePartly supported

  The Results and Discussion report that some C. auris isolates form aggregates, apparently because daughter cells are not liberated after budding, and that vigorous vortex mixing and detergent did not disrupt them. The paper does not identify those cells as lacking ACE2 or establish ACE2 loss as the cause; its physical-disruption finding is limited to the tested aggregates. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: C. auris clinical isolates' morphologies and mannan structures studied are representative of clinical C. auris strains.

In both epicutaneous colonization and intradermal infection mouse models, C. auris induces the accumulation of CD4+ IL-17A+ and CD4+ IL-17F+ Th17 cells in the skin.

“In both epicutaneous colonization and intradermal infection mouse models, C. auris induces the accumulation of CD4+ IL-17A+ and CD4+ IL-17F+ Th17 cells in the skin [3,85].”

• cites [3] X Huang, 2021, Murine model of colonization with fungal pathogen Candida auris to explore skin tropism, host risk factors and therapeutic strategies, Cell Host Microbe sourcePartly supported

  The Results section, “Skin Association with C. auris Promotes a Protective IL-17A/IL-17F Response” (page not provided), reports accumulation of CD4+ IL-17A+ and CD4+ IL-17F+ Th17 cells after topical skin association. It does not establish the same finding in an intradermal infection model; the Methods describe topical application for the skin-colonization experiments. (LLM, conf=0.88)

  Experimental — accuracy not yet measured
• cites [85] A Datta, 2023, Differential skin immune responses in mice intradermally infected with Candida auris and Candida albicans, Microbiol Spectr sourceSupported

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

Yeast, filamentous, and aggregative forms of C. auris elicit distinct magnitudes of Th17 activation, likely reflecting differences in cell wall composition and surface antigen exposure.

“Collectively, yeast, filamentous, and aggregative forms of C. auris elicit distinct magnitudes of Th17 activation, likely reflecting differences in cell wall composition and surface antigen exposure (Fig 4) [87,113].”

• cites [87] MV Horton, 2021, Candida auris cell wall mannosylation contributes to neutrophil evasion through pathways divergent from Candida albicans and Candida glabrata, mSphere sourcePartly supported

  The Results section on pathogen-associated molecular patterns reports that disrupting C. auris mannosylation increases cell-surface β-glucan and chitin exposure. It does not compare yeast, filamentous, and aggregative forms or report Th17 activation, so it supports only the cell-wall-exposure rationale, not the claimed differences among forms. (LLM, conf=0.82)

  Experimental — accuracy not yet measured
• cites [113] Y Wang, 2022, Innate immune responses against the fungal pathogen Candida auris, Nat Commun sourcePartly supported

  The Introduction and cell-wall Results section link differences in C. auris cell-wall structure and antigen exposure to innate immune recognition. But the morphology Results section reports no difference in the measured cytokine responses among yeast, filamentation-competent yeast, and filamentous cells (Fig. 4a); it does not assess aggregative forms or Th17 activation. The claimed differences in Th17 activation among the three forms are therefore not supported by this paper. (LLM, conf=0.82)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.
• AssumptionRests on an assumption: C. auris clinical isolates' morphologies and mannan structures studied are representative of clinical C. auris strains.

During S. aureus subcutaneous infection in mice, dermal fibroblasts undergo reactive adipogenesis and expand as preadipocytes that secrete CAMP.

“During S. aureus subcutaneous infection in mice, dermal fibroblasts undergo reactive adipogenesis and expand as preadipocytes that secrete CAMP (Cathelicidin Antimicrobial Peptide) [97].”

• cites [97] L Zhang, 2015, Innate immunity. Dermal adipocytes protect against invasive Staphylococcus aureus skin infection, Science sourcePartly supported

  The paper reports preadipocyte proliferation and dermal-fat expansion after S. aureus skin infection in mice. It also finds cathelicidin production during adipocyte differentiation, but does not establish that dermal fibroblasts become preadipocytes; the infected cells colocalized with a fibroblast marker. Its secretion experiments used differentiating or differentiated adipocytes, not undifferentiated preadipocytes (indexed copy, section labeled Abstract; page unavailable). (LLM, conf=0.86)

  Experimental — accuracy not yet measured

In a murine model of intradermal infection, the ace2Δ mutant strain of C. auris induces greater Th17 responses compared to wild-type or complemented strains.

“In a murine model of intradermal infection, the ace2Δ mutant strain of C. auris induced greater Th17 responses compared to wild-type or complemented strains [109].”

• cites [109] A Balakumar, 2024, Cell aggregation mediated by ACE2 deletion in Candida auris modulates fungal colonization and host immune responses in the skin, mSphere sourceSupported

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.
• AssumptionRests on an assumption: C. auris clinical isolates' morphologies and mannan structures studied are representative of clinical C. auris strains.

The aggregative phenotype of C. auris is controlled at least in part by the zinc-finger transcription factor ACE2 that governs cell separation via the chitinase CST1.

“Additional studies recently examined how the aggregative phenotype of C. auris, a complex phenomenon controlled at least in part by the zinc-finger transcription factor ACE2 that governs cell separation via the chitinase CST1, regulates Th17 cell development [109,110].”

• cites [109] A Balakumar, 2024, Cell aggregation mediated by ACE2 deletion in Candida auris modulates fungal colonization and host immune responses in the skin, mSphere sourcePartly supported

  The Introduction identifies ACE2 as a zinc-finger transcription factor involved in C. auris aggregation and cell separation. It names the chitinase whose expression ACE2 controls as CTS1, however, not CST1 as the claim states. (LLM, conf=0.90)

  Experimental — accuracy not yet measured
• cites [110] D Malavia-Jones, 2023, Strain and temperature dependent aggregation of Candida auris is attenuated by inhibition of surface amyloid proteins, Cell Surf sourcePartly supported

  The Introduction reports that ACE2 deletion was associated with reduced expression of the chitinase CTS1, which might contribute to cell-separation defects and aggregation. But the Results found no correlation between CTS1 expression and aggregation, and the Discussion says cell-separation defects did not explain aggregation differences in the isolates studied. The claim presents a tentative mechanism as established and names the chitinase CST1 rather than CTS1. (LLM, conf=0.87)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: C. auris clinical isolates' morphologies and mannan structures studied are representative of clinical C. auris strains.

Clinical isolates of C. auris exhibit distinct morphologies, including yeast, aggregative, and filamentous.

“Clinical isolates of C. auris exhibit distinct morphologies, including yeast, aggregative, and filamentous [104–108].”

• cites [104] DJ Santana, 2021, Forward and reverse genetic dissection of morphogenesis identifies filament-competent Candida auris strains, Nat Commun sourceSupported
• cites [105] S Fan, 2021, Filamentous growth is a general feature of Candida auris clinical isolates, Med Mycol sourceNot checked — no full text of the source
• cites [106] JL Brown, 2020, Candida auris phenotypic heterogeneity determines pathogenicity in vitro, mSphere sourcePartly supported

  The Results and Materials and Methods classify clinical isolates as aggregative or nonaggregative, and the Discussion describes individual yeast cells mixed with aggregates. The Discussion says true hyphal formation is absent in the biofilms studied, although it can be induced under some conditions. The paper therefore does not establish filamentous clinical isolates as a third morphology alongside the two phenotypes it examined. (LLM, conf=0.86)

  Experimental — accuracy not yet measured
• cites [107] H Du, 2020, Candida auris: Epidemiology, biology, antifungal resistance, and virulence, PLoS PathogNot checked yet

  Not checked in the free run.

• cites [108] G Bryak, 2024, Yeast and filamentous Candida auris stimulate distinct immune responses in the skin, mSphere sourcePartly supported

  The OBSERVATION section (page not provided) says clinical isolates can exhibit yeast and filamentous forms, alongside pseudohyphal forms. It does not identify an aggregative morphotype, so that item in the cited list is not supported by our copy. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: C. auris clinical isolates' morphologies and mannan structures studied are representative of clinical C. auris strains.

Skin fibroblast subsets express a broad array of cytokines, chemokines, PRRs, and AMPs in response to C. auris.

“Skin fibroblast subsets also expressed a broad array of cytokines, chemokines, PRRs, and AMPs in response to C. auris, including Il33, Csf1, Tgfb2, Ccl2, Ccl7, Ccl11, Cxcl1, Cxcl5, Cxcl9, Cxcl10, Cxcl12, Cxcl14, Clec3b, Clec11a, Nod1, Mrc2, Lgals1, Lgals9, Lman1, Lnc2, Adm and Ang [86].”

• cites [86] A Balakumar, 2024, Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris, PLoS Pathog sourcePartly supported

  The Results section on fibroblast transcriptomic signatures (Figure 4C–D; page not provided) reports cytokines, chemokines, fungal-recognizing receptors, and antimicrobial peptides in fibroblast subsets during C. auris skin infection, supporting the main claim and most listed genes. The cited fibroblast passage specifies Nod2, not Nod1, and Lcn2, not the citing sentence’s Lnc2; the paper reports Nod1 in myeloid cells instead. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

A broader spectrum of cutaneous stromal cells is identified with a dynamic transcriptional program during C. auris infection.

“A broader spectrum of cutaneous stromal cells was also identified with a dynamic transcriptional program during C. auris infection (Fig 3).”

• cites [86] A Balakumar, 2024, Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris, PLoS Pathog sourceSupported

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

IL-17A/IL-17F responses are critical for cutaneous protection against C. auris colonization.

“Using Act1-deficient mice lacking IL-17 receptor signaling, Huang and colleagues showed that IL-17A/IL-17F responses are critical for cutaneous protection against C. auris colonization (Fig 4) [3].”

• cites [3] X Huang, 2021, Murine model of colonization with fungal pathogen Candida auris to explore skin tropism, host risk factors and therapeutic strategies, Cell Host Microbe sourceSupported

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

C. auris elicits protective IL-17 immunity through Card9- and LC-independent pathways during colonization of the skin.

“Moreover, whereas LCs promote the induction of Th17 cells during C. albicans skin infection [103], LC-deficient mice controlled C. auris colonization normally, collectively indicating that C. auris elicits protective IL-17 immunity through Card9- and LC-independent pathways during colonization of the skin [3].”

• cites [3] X Huang, 2021, Murine model of colonization with fungal pathogen Candida auris to explore skin tropism, host risk factors and therapeutic strategies, Cell Host Microbe sourcePartly supported

  The Results section ('Skin Association with C. auris Promotes a Protective IL-17A/IL-17F Response'; page not supplied) reports a protective IL-17 response and normal control of skin colonization in mice deficient in Langerhans cells or Card9. It only suggests that these factors may not be implicated in the overall IL-17 response; it does not establish the claimed Card9- and LC-independent pathways. (LLM, conf=0.84)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

Clinical isolates of C. auris that harbor ACE single-nucleotide polymorphisms form rough, adherent colonies.

“Recent reports showed that clinical isolates of C. auris that harbor ACE single-nucleotide polymorphisms form rough, adherent colonies [112].”

• cites [112] S Tian, 2023, Phenotypic and genetic features of a novel clinically isolated rough morphotype Candida auris, Front Microbiol sourcePartly supported

  The Results (Microbiological characteristics; Phylogenetic analysis) describe two clinical rough-morphotype isolates with ACE2 mutations and tightly connected, aggregating cells. They do not establish that the colonies are adherent, and the Discussion says further experiments are needed to determine whether the ACE2 mutation is associated with the rough phenotype. The paper identifies the gene as ACE2, not ACE. (LLM, conf=0.84)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: C. auris clinical isolates' morphologies and mannan structures studied are representative of clinical C. auris strains.

In an intradermal mouse model of C. auris skin infection, scRNA-seq identifies a fibroblast subset expressing adipocyte lineage markers as the only proliferating non-immune cell population.

“Utilizing an intradermal mouse model of C. auris skin infection, scRNA-seq identified a fibroblast subset expressing adipocyte lineage markers as the only proliferating non-immune cell population [83], suggesting an analogous reactive adipogenesis during cutaneous C. auris infection.”

• cites [83] JV Desai, 2018, The role of neutrophils in host defense against invasive fungal infections, Curr Clin Microbiol Rep sourceCould not verify

  The cited review’s sections on Candida albicans and Aspergillus infections discuss neutrophil recruitment and antifungal activity, not the claimed C. auris skin model. Searches for intradermal C. auris infection, scRNA-seq, adipocyte-lineage fibroblasts, and proliferating non-immune cells found no passage addressing the claim in our copy. (LLM, conf=0.76)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

Non-immune stromal cells mount a coordinated innate response during C. auris infection, coupling structural maintenance with immune activation.

“Together, these findings demonstrate that non-immune stromal cells mount a coordinated innate response during C. auris infection, coupling structural maintenance with immune activation.”

• cites [83] JV Desai, 2018, The role of neutrophils in host defense against invasive fungal infections, Curr Clin Microbiol Rep sourceCould not verify

  The sections on anti-Candida albicans and anti-Aspergillus fumigatus neutrophil effector functions discuss immune-cell interactions, not a stromal-cell response to C. auris. Searches for C. auris, non-immune stromal cells, and structural maintenance found no passage addressing the attributed claim. No page numbers were provided in our copy. (LLM, conf=0.76)

  Experimental — accuracy not yet measured
• cites [86] A Balakumar, 2024, Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris, PLoS Pathog sourcePartly supported

  The Results section on fibroblasts and other non-immune cells reports increased expression of immune-related genes during C. auris skin infection and enrichment of an ECM–receptor interaction pathway in one fibroblast subset. The Discussion likewise suggests an active defensive role for non-immune cells. These transcriptomic findings do not demonstrate structural maintenance or establish that it is coordinated with immune activation. (LLM, conf=0.84)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

Depletion of IL-12-producing inflammatory macrophages and monocyte-derived dendritic cells with clodronate liposome or in Ccr2−/− mice decreases IL-12 production and Th1 cell development in vivo.

“Indeed, depletion of these populations with clodronate liposome or Ccr2−/− mice decreased IL-12 production and Th1 cell development in vivo [122].”

• cites [122] R Feuerstein, 2020, Resident macrophages acquire innate immune memory in staphylococcal skin infection, Elife sourcePartly supported

  The Results section, “Resident dermal Mφ mediate innate memory” (page not available), reports that clodronate liposomes depleted resident dermal macrophages. The Results section on infection-induced resistance (page not available) reports reduced inflammatory monocytes in Ccr2−/− mice. Neither passage reports depletion of monocyte-derived dendritic cells or a decrease in IL-12 production or Th1-cell development; the measured outcomes were bacterial killing, infiltrating cells, and IL-1β. (LLM, conf=0.84)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

IL-12-producing inflammatory macrophages and monocyte-derived dendritic cells are the key sources of IFN-γ-inducing signals during C. auris re-infection.

“At the cellular level, IL-12-producing inflammatory macrophages and monocyte-derived dendritic cells are the key sources of IFN-γ-inducing signals during C. auris re-infection (Fig 4).”

• cites [122] R Feuerstein, 2020, Resident macrophages acquire innate immune memory in staphylococcal skin infection, Elife sourceCould not verify

  The Results sections on dermal macrophage responses and secondary infection describe an S. aureus mouse model, not C. auris re-infection. Searches for IL-12, IFN-γ and monocyte-derived dendritic cells did not yield a passage identifying the claimed sources of IFN-γ-inducing signals. (LLM, conf=0.78)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

Anti-C. albicans host defense mechanisms cannot be directly extrapolated to C. auris given major cell wall differences between the species.

“they cannot be directly extrapolated to C. auris given these major cell wall differences between the species.”

Exposure to antifungals may be a possible risk factor for C. auris colonization and infection in hospitalized patients.

“These findings suggest that exposure to antifungals may be a possible risk factor for C. auris colonization and infection in hospitalized patients.”

Alteration of the skin microbiome by broad-spectrum antibiotics may create a permissive environment for C. auris to colonize.

“This alteration in the microbiome may create a permissive environment for C. auris to colonize.”

The age of the individual has been reported as a predisposing factor for C. auris skin colonization in some studies, with C. auris-colonized patients aged 65-80 years at greater risk.

“The age of the individual has been reported as a predisposing factor for C. auris skin colonization in some studies, with C. auris-colonized patients aged 65–80 years at greater risk [62–64].”

• cites [62] J Rogers, 1996, Stratum corneum lipids: the effect of ageing and the seasons, Arch Dermatol Res sourceNot checked — no full text of the source
• cites [63] M Takahashi, 2004, The content of free amino acids in the stratum corneum is increased in senile xerosis, Arch Dermatol Res sourceNot checked — no full text of the source
• cites [64] A Abdolrasouli, 2017, In vitro efficacy of disinfectants utilised for skin decolonisation and environmental decontamination during a hospital outbreak with Candida auris, Mycoses sourceNot checked — no full text of the source

Obesity is associated with C. auris infection in certain clinical studies.

“which may help explain the association between obesity and C. auris infection in certain clinical studies [44].”

• cites [44] K Vinayagamoorthy, 2022, Prevalence, risk factors, treatment and outcome of multidrug resistance Candida auris infections in Coronavirus disease (COVID-19) patients: a systematic review, Mycoses sourceNot checked — no full text of the source

Systemic antibiotic administration, such as doxycycline and trimethoprim/sulfamethoxazole (TMP/SMX), can penetrate the dermis and epidermis, altering the skin bacterial microbiome and enriching antibiotic-resistant strains.

“Jo and colleagues demonstrated that systemic antibiotic administration, such as doxycycline and trimethoprim/sulfamethoxazole (TMP/SMX), can penetrate the dermis and epidermis, altering the skin bacterial microbiome and enriching antibiotic-resistant strains [50].”

• cites [50] NISC Comparative Sequencing Program, 2021, Alterations of human skin microbiome and expansion of antimicrobial resistance after systemic antibiotics, Sci Transl MedNot checked yet

  Not checked in the free run.

The skin of older individuals shows reduced lipid content and natural moisturizing factors, which are essential for maintaining an effective stratum corneum barrier.

“The skin of older individuals also shows reduced lipid content and natural moisturizing factors, which are essential for maintaining an effective stratum corneum barrier [62,63].”

• cites [62] J Rogers, 1996, Stratum corneum lipids: the effect of ageing and the seasons, Arch Dermatol Res sourceNot checked — no full text of the source
• cites [63] M Takahashi, 2004, The content of free amino acids in the stratum corneum is increased in senile xerosis, Arch Dermatol Res sourceNot checked — no full text of the source

The gene expression of SCF1 and ALS4112 across C. auris clades and strains may affect their skin colonization potential.

“This suggests that the gene expression of SCF1 and ALS4112 across C. auris clades and strains may affect their skin colonization potential.”

Differential fungal factors and their gene expression across clades may contribute to variable propensities for C. auris skin colonization.

“This shows that differential fungal factors and their gene expression across clades may contribute to variable propensities for C. auris skin colonization.”

Macrophage depletion in murine C. auris skin infection markedly reduces fungal burden.

“In vivo, macrophage depletion in murine C. auris skin infection markedly reduced fungal burden.”

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

Hog1-dependent stress tolerance is critical for both cutaneous and systemic spread of C. auris.

“Thus, Hog1-dependent stress tolerance is critical for both cutaneous and systemic spread of C. auris.”

• AssumptionRests on an assumption: Findings from murine and ex vivo skin models of C. auris colonization and infection are relevant to human C. auris skin colonization and infection.

This metabolic adaptation of C. auris may favor long-term persistence in the skin.

“This metabolic adaptation of C. auris may favor long-term persistence in the skin.”

C. auris infection preferentially induces IFN-γ-secreting pathogenic Th1 cells upon re-infection.

“Recent studies have shown that C. auris infection preferentially induces IFN-γ-secreting pathogenic Th1 cells upon re-infection (Fig 4) [115,116].”

• cites [115] D Das, 2025, The emerging fungal pathogen Candida auris induces IFNγ to colonize the skin, PLoS PathogNot checked yet

  Not checked in the free run.

• cites [116] Merrill ED. The emerging fungal pathogen Candida auris induces IFNgamma to colonize mammalian hair follicles. 2025. Available from: https://www.biorxiv.org/content/10.1101/2025.01.15.632653v1.full sourceNot checked — no full text of the source

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

Endothelial cells upregulate several neutrophil chemoattractant molecules during C. auris skin infection, likely supporting neutrophil extravasation and recruitment from the blood to the infected tissue.

“Endothelial cells, likewise, upregulate several neutrophil chemoattractant molecules during C. auris skin infection, likely supporting neutrophil extravasation and recruitment from the blood to the infected tissue.”

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

Keratinocyte-specific IFNγR1 conditional knockout mice are protected from barrier damage and fungal proliferation and persistence in vivo.

“Consistently, keratinocyte-specific IFNγR1 conditional knockout mice were protected from barrier damage and fungal proliferation and persistence in vivo [116].”

• cites [116] Merrill ED. The emerging fungal pathogen Candida auris induces IFNgamma to colonize mammalian hair follicles. 2025. Available from: https://www.biorxiv.org/content/10.1101/2025.01.15.632653v1.full sourceNot checked — no full text of the source

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

Excess IFN-γ partially attenuates protective IL-17-mediated responses following secondary infection with C. auris, thereby promoting persistence.

“These findings suggest that excess IFN-γ partially attenuates protective IL-17-mediated responses following secondary infection with C. auris, thereby promoting persistence.”

• cites [115] D Das, 2025, The emerging fungal pathogen Candida auris induces IFNγ to colonize the skin, PLoS PathogNot checked yet

  Not checked in the free run.

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.

Ifng-/- mice display lower fungal burden associated with increased Th17 cells and expression of IL-17 receptor-dependent genes such as Cxcl1, S100a8, Il6, and Il1b.

“First, Ifng-/- mice displayed lower fungal burden associated with increased Th17 cells and expression of IL-17 receptor-dependent genes such as Cxcl1, S100a8, Il6, and Il1b.”

• cites [115] D Das, 2025, The emerging fungal pathogen Candida auris induces IFNγ to colonize the skin, PLoS PathogNot checked yet

  Not checked in the free run.

• AssumptionRests on an assumption: Findings from murine models of C. auris skin infection are representative of human skin infection.