Innate immune responses against the fungal pathogen Candida auris
Open accessAbstract
Candida auris is a multidrug-resistant human fungal pathogen responsible for nosocomial outbreaks worldwide. Although considerable progress has increased our understanding of the biological and clinical aspects of C. auris, its interaction with the host immune system is only now beginning to be investigated in-depth. Here, we compare the innate immune responses induced by C. auris BJCA001 and Candida albicans SC5314 in vitro and in vivo. Our results indicate that C. auris BJCA001 appears to be less immunoinflammatory than C. albicans SC5314, and this differential response correlates with structural features of the cell wall.
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C. auris differentially stimulates cytokine production in peripheral blood mononuclear cells compared to C. albicans.
“C. auris differentially stimulates cytokine production in peripheral blood mononuclear cells, decreases phagocytosis by neutrophils, and has a more potent binding to IgG than C. albicans [13–15].”
From The Emerging Fungal Pathogen Candida auris Induces IFNγ to Colonize the Skin (2025) · cites this paper as [13]
The Results section reports that some C. auris strains elicited more cytokine production from human PBMCs than C. albicans, with higher TNF-α for all tested C. auris strains only at high MOI. It also says that most comparisons showed the same pattern of increased responsiveness to either species, so the unqualified claim overstates how consistently their effects differed. (LLM, conf=0.88)
Experimental — accuracy not yet measuredDifferences in mannan composition between C. auris and C. albicans contribute to decreased innate immune recognition, phagocytic activity, and clearance of C. auris in human neutrophils.
“Recent evidence indicates that differences in mannan composition between C. auris and C. albicans contribute to decreased innate immune recognition, phagocytic activity, and clearance of C. auris in human neutrophils (13, 27, 28).”
From Differential skin immune responses in mice intradermally infected with <i>Candida auris</i> and <i>Candida albicans</i> (2023) · cites this paper as [13]
The Results report that C. auris was taken up by human and mouse neutrophils at lower rates than C. albicans, while the cell-wall comparison links distinct mannan structure to reduced innate immune recognition. The paper’s proposed mannan mechanism focuses on macrophages; it does not directly establish that the between-species mannan difference causes reduced phagocytosis or clearance by human neutrophils. (LLM, conf=0.84)
Experimental — accuracy not yet measuredC. auris differentially stimulates cytokine production in peripheral blood mononuclear cells and has a more potent binding to IgG than C. albicans.
“C. auris differentially stimulates cytokine production in peripheral blood mononuclear cells and has a more potent binding to IgG than C. albicans [14, 15].”
From Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris (2024) · cites this paper as [14]
The Results section on PBMC responses reports that C. auris sometimes elicited more cytokine production than C. albicans, although most tests showed similar responses. Our copy does not establish stronger IgG binding by C. auris than by C. albicans; IgG binding appears in the title of a work listed in the References, without that comparison. (LLM, conf=0.87)
Experimental — accuracy not yet measuredIn recent studies on the host transcriptome of C. auris in human PBMCs and mouse BMDMs, the NOD-like receptor signaling pathway was only enriched in C. auris infection but not in C. albicans infection.
“In the recent studies on the host transcriptome of C. auris in human peripheral blood mononuclear cells (PBMCs) and mouse BMDMs, the NOD-like receptor signaling pathway was only enriched in the C. auris infection but not in C. albicans infection [13, 14]”
From Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris (2024) · cites this paper as [14]
The Results section on in vitro cell culture reports RNA-seq and pathway-enrichment analysis in mouse BMDMs challenged with C. auris or C. albicans. It does not report that NOD-like receptor signaling was enriched only with C. auris; the pathways it identifies as specific to one infection are instead associated with C. albicans. The paper also examines human PBMC cytokine production, but the cited passages do not establish the claimed PBMC transcriptome finding. (LLM, conf=0.82)
Experimental — accuracy not yet measuredYeast, 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].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [113]
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
C. auris decreases phagocytosis by neutrophils compared to C. albicans.
“C. auris differentially stimulates cytokine production in peripheral blood mononuclear cells, decreases phagocytosis by neutrophils, and has a more potent binding to IgG than C. albicans [13–15].”
From The Emerging Fungal Pathogen Candida auris Induces IFNγ to Colonize the Skin (2025) · cites this paper as [13]
C. auris elicits less potent innate immune responses compared to C. albicans in the mouse model of systemic infection.
“Recent evidence indicates that C. auris elicits less potent innate immune responses compared to C. albicans in the mouse model of systemic infection (13).”
From Differential skin immune responses in mice intradermally infected with <i>Candida auris</i> and <i>Candida albicans</i> (2023) · cites this paper as [13]
Neutrophils are less efficient in recognizing and killing C. auris due to the presence of a dense mannan layer and recruit significantly fewer neutrophils than C. albicans in the murine infection.
“Recent evidence suggests that neutrophils are less efficient in recognizing and killing C. auris (29) due to the presence of a dense mannan layer (30) and recruit significantly fewer neutrophils than the C. albicans in the murine infection (5, 31).”
From Cell aggregation mediated by <i>ACE2</i> deletion in <i>Candida auris</i> modulates fungal colonization and host immune responses in the skin (2024) · cites this paper as [31]
Increased β-glucan in cell wall mannosylation mutant strains is associated with enhanced fungal killing by neutrophils and macrophages.
“was associated with enhanced fungal killing by neutrophils and macrophages (62, 63).”
From The <i>Candida auris</i> Hog1 MAP kinase is essential for the colonization of murine skin and intradermal persistence (2024) · cites this paper as [62]
C. auris has more potent binding to IgG than C. albicans.
“C. auris differentially stimulates cytokine production in peripheral blood mononuclear cells, decreases phagocytosis by neutrophils, and has a more potent binding to IgG than C. albicans [13–15].”
From The Emerging Fungal Pathogen Candida auris Induces IFNγ to Colonize the Skin (2025) · cites this paper as [13]
The Discussion describes differences in innate immune recognition, and the Results compare cell-wall structure, but neither reports that C. auris binds IgG more strongly than C. albicans. A paper about selective IgG binding appears in the References (ref. 57); its title alone does not establish the comparative claim in this source. Searches for “IgG” and comparative IgG binding found no supporting passage. (LLM, conf=0.74)
Experimental — accuracy not yet measured
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Stable peptide-assembled nanozyme mimicking dual antifungal actions
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Self-citationRapid evolution of an adaptive multicellular morphology of Candida auris during systemic infection
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Self-citationMechanisms of pathogenicity for the emerging fungus Candida auris
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Role of Microbiota in the Skin Colonization of Candida auris
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Candida auris undergoes adhesin-dependent and -independent cellular aggregation
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Candidiasis: Insights into Virulence Factors, Complement Evasion and Antifungal Drug Resistance
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Sugar symphony: glycosylation in cancer metabolism and stemness
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“albicans in the mouse model of systemic infection (13).”
BackgroundNative human and mouse skin infection models to study Candida auris-host interactions
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<i>Candida auris</i> —macrophage cellular interactions and transcriptional response
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Targeting Fks1 proteins for novel antifungal drug discovery
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Uniqueness of Candida auris cell wall in morphogenesis, virulence, resistance, and immune evasion
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Candida Infections: The Role of Saliva in Oral Health—A Narrative Review
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Small molecules for combating multidrug-resistant superbug Candida auris infections
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Self-citationHost immune response against fungal biofilms
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Self-citationThe Emerging Fungal Pathogen Candida auris Induces IFNγ to Colonize the Skin
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Innate immune response to Candida auris
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Resilience in Resistance: The Role of Cell Wall Integrity in Multidrug-Resistant Candida
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Yeast and filamentous <i>Candida auris</i> stimulate distinct immune responses in the skin
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Research advances and public health strategies in China on WHO priority fungal pathogens
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Self-citationDiscovery of a new chemical scaffold for the treatment of superbug Candida auris infections
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Candida auris : host interactions, antifungal drug resistance, and diagnostics
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Tools and techniques to identify, study, and control Candida auris
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The hidden threat: Unveiling the rise of antifungal drug resistance
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Self-citationInnate Immune Responses to Sporothrix schenckii: Recognition and Elimination
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A broad-spectrum anti-fungal effector dictates bacterial-fungal interkingdom interactions
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Impact of Micafungin on Candida auris β-glucan Masking and Neutrophil Interactions
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Vertebrate and invertebrate animal infection models of Candida auris pathogenicity
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Synthesis and antifungal evaluation of novel triazole derivatives bearing a pyrazole-methoxyl moiety
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Pathobiology of Candida auris infection analyzed by multiplexed imaging and single cell analysis
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Host defense mechanisms against Candida auris
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CVF1 Promotes Invasive Candida albicans Infection via Inducing Ferroptosis
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Self-citationThe emerging pathogen Candida auris: host interactions and disease drivers
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Growth phase influences virulence in Candidozyma auris systemic infection models
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Carbon Dioxide Controls Fungal Fitness and Skin Tropism of Candida aurisPreprint
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Host–Candida auris interactions in the skin
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Candida auris adhesins, specifically Als3, a key target to understand and mitigate
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Self-citationZCF4-dependent suppression of MMP-9 drives virulence in fluconazole-resistant Candida auris
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Self-citationCandida auris uses nutrient sensing to modulate virulence and host immune responses
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A synergistic antifungal strategy using multifunctional nanoplatform for vaginitis therapy
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Adaptor protein CARD9 is required for systemic host defense against Candida auris
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Human keratinocytes and fibroblasts coordinate early cutaneous innate defenses against Candida auris
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Seaside to Bedside: Assembly in Research for Emerging Human Fungal Pathogen Candida auris
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Candida Auris : What do We Know about the Most Enigmatic Pathogen of the 21 st Century?
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Self-citationMolecular mechanism of host-yeast interactions and prevention by nanoformulation approaches
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Fungicidal Efficacy of Amphotericin B and Micafungin Against Candida auris Within Macrophage
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EPHA5 regulates antifungal innate immunity by phosphorylating EPHB2 and Dectin-1
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- Authors
- Wang, Y., Zou, Y., Chen, X., Li, H., Yin, Z., Zhang, B., Xu, Y., Zhang, Y., Zhang, R., Huang, X., Yang, W., Xu, C., Jiang, T., Tang, Q., Zhou, Z., Ji, Y., Liu, Y., Hu, L., Zhou, J., Zhou, Y., Zhao, J., Liu, N., Huang, G., Chang, H., Fang, W., Chen, C., & Zhou, D.
- Affiliations
- Chinese Academy of Sciences (CN)
- Shanghai Jiao Tong University (CN)
- Beijing Institute of Microbiology and Epidemiology (CN)
- Shanghai University of Traditional Chinese Medicine (CN)
- Jiangnan University (CN)
- Shanghai University (CN)
- Tongji University (CN)
- Gannan Medical University (CN)
- Guangxi Academy of Sciences (CN)
- Fudan University (CN)
- Corresponding author
- Chen, Changbin
- Zhou, Dongsheng
- ORCID
- Venue
- Nature Communications
- Published
- 2022-06-21
- Volume
- 13
- Issue
- 1
- Pages
- 3553-3553
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC9213489
- OpenAlex
- W4283321860
- Cited by
- 107
- References
- 70
- Citations by year
- 2026: 26 · 2025: 27 · 2024: 32 · 2023: 18 · 2022: 4
- FWCI
- 9.90
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Natural Science Foundation of Shanghai (2019SHZDZX02, 20ZR1463800)
- National Natural Science Foundation of China (31600119, BM2020019, 2020YFA0907200, 2019SHZDZX02, 32070146, 32170195, 31870141)
- Chinese Academy of Sciences (153831KYSB20170043, KGFZD-135-19-11)
- Government of Jiangsu Province
- Youth Innovation Promotion Association of the Chinese Academy of Sciences (31600119)
- State Key Laboratory of Pathogen and Biosecurity
- Youth Innovation Promotion Association
- Institute of Microbiology, Chinese Academy of Sciences
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Health Sciences › Medicine › Epidemiology › Fungal Infections and Studies
- Keywords
- Candida auris, innate immunity, Candida albicans, fungal pathogen-host interaction, immune inflammation, cell wall structure, multidrug resistance, hospital outbreak
- MeSH terms
- Candida auris, Antifungal Agents, Candida, Candida albicans, Candidiasis, Humans, Immunity, Innate, Microbial Sensitivity Tests
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