Candida auris cell wall mannosylation contributes to neutrophil evasion through pathways divergent from candida albicans and candida glabrata
Open accessAbstract
The emerging fungal pathogen Candida auris presents a global public health threat. Therapeutic options are often limited for this frequently drug-resistant pathogen, and mortality rates for invasive disease are high.
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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.
“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 [28]
The Results report that disrupting C. auris mannosylation increased engagement, phagocytosis, and killing by human neutrophils; the Discussion says neutrophils engage C. albicans more readily than C. auris. However, the paper does not establish that differences in mannan composition *between the species* cause the difference in neutrophil recognition or clearance. Its proposed mechanism centers on C. auris mannan masking other cell-wall components. (LLM, conf=0.85)
Experimental — accuracy not yet measuredIncreased β-glucan in cell wall mannosylation mutant strains enhances neutrophil recruitment in a zebrafish infection model.
“The increased β-glucan in the cell wall mannosylation mutant strains has been shown to enhance neutrophil recruitment in a zebrafish infection model (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 [63]
The Results sections on cell-surface PAMPs and zebrafish recruitment report that C. auris pmr1Δ and van1Δ mutants expose more β-glucan and recruit more neutrophils to the larval zebrafish hindbrain than wild type. The paper also reports increased chitin exposure and does not show that β-glucan specifically caused the increased recruitment. Page numbers are unavailable in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIncreased 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 [63]
The Results sections on phagocytosis and cell-surface pathogen-associated molecular patterns report that C. auris mannosylation mutants expose more β-glucan and are more susceptible to killing by neutrophils. The zebrafish Results section reports similar macrophage recruitment to wild-type and mutant strains, but does not report enhanced killing by macrophages. The macrophage-killing part of the claim is therefore unsupported by this paper. (LLM, conf=0.90)
Experimental — accuracy not yet measuredThe 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.”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [87]
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 measuredC. auris uses a two-tiered evasion strategy: it masks immunogenic β-glucan through mannosylation to avoid neutrophil recognition and simultaneously induces macrophage-derived IL-1Ra to suppress IL-1R-dependent neutrophil recruitment and activation.
“Together, these findings uncover a two-tiered evasion strategy: C. auris masks immunogenic β-glucan through mannosylation to avoid neutrophil recognition and simultaneously induces macrophage-derived IL-1Ra to suppress IL-1R-dependent neutrophil recruitment and activation.”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [87]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measured
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].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [87]
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 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 [87]
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 measuredC. 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 [15]
Cell wall mannan plays a role in neutrophil evasion by masking both glucan and chitin PAMPs.
“Cell wall mannan has also been shown to play a role in neutrophil evasion by masking both glucan and chitin PAMPs (21, 24).”
From Dual function of <i>Candida auris</i> mannosyltransferase, MNT5, in biofilm community protection from antifungal therapy and the host (2025) · cites this paper as [24]
Neutrophils are less effective at engaging, phagocytosing, and killing C. auris when compared to C. albicans.
“However, neutrophils are less effective at engaging, phagocytosing, and killing C. auris when compared to C. albicans (21, 24).”
From Dual function of <i>Candida auris</i> mannosyltransferase, MNT5, in biofilm community protection from antifungal therapy and the host (2025) · cites this paper as [24]
Growth kinetics was unaltered in C. auris pmr1Δ.
“The growth kinetics was unaltered in C. auris pmr1Δ [34]”
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 [30]
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].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [87]
Wild-type C. auris resists neutrophil killing, whereas deletion of PMR1 and VAN1 in C. albicans and C. glabrata does not alter their engagement with neutrophils, highlighting a species-specific role for C. auris mannosylation in neutrophil evasion.
“Correspondingly, wild-type C. auris resisted neutrophil killing, whereas deletion of PMR1 and VAN1 in C. albicans and C. glabrata did not alter their engagement with neutrophils, thereby highlighting a species-specific role for C. auris mannosylation in neutrophil evasion [87].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [87]
C. auris neutrophil evasion is linked to its cell wall mannosylation.
“Recent work linked this neutrophil evasion to C. auris cell wall mannosylation [87].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [87]
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].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [87]
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 [15]
The Results section reports reduced neutrophil phagocytosis of C. auris relative to C. albicans, but does not compare their binding to IgG. The IgG mentioned in the Results and fluorescent-labeling Methods is an anti-human IgG Fc antibody used to detect a dectin-1 reagent, not a measurement of Candida–IgG binding (page unavailable). Searches for IgG binding, immunoglobulin, and opsonization found no passage addressing the claimed comparison. (LLM, conf=0.75)
Experimental — accuracy not yet measuredC. 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 [15]
The Results section compares C. auris and C. albicans in neutrophil phagocytosis assays, not cytokine production in peripheral blood mononuclear cells. Searches for PBMCs and cytokine production found no passage in our copy addressing that comparison; the cited paper therefore does not verify the specific claim. (LLM, conf=0.73)
Experimental — accuracy not yet measured
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Cites
Novel Entries in a Fungal Biofilm Matrix Encyclopedia
Zarnowski, R., Westler, W. M., Lacmbouh, G. A., Marita, J. M., Bothe, J. R., Bernhardt, J., Lounes-Hadj Sahraoui, A., Fontaine, J., Sanchez, H., Hatfield, R. D., et al. (2014) · mBio · doi:10.1128/mbio.01333-14 · Cited by 315 · see citing works
Self-citationSherrington, S. L., Sorsby, E., Mahtey, N., Kumwenda, P., Lenardon, M. D., Brown, I., Ballou, E. R., MacCallum, D. M., & Hall, R. A. (2017) · PLOS Pathogens · doi:10.1371/journal.ppat.1006403 · Cited by 202 · see citing works
Unique Cell Surface Mannan of Yeast Pathogen <i>Candida auris</i> with Selective Binding to IgG
Yan, L., Xia, K., Yu, Y., Miliakos, A., Chaturvedi, S., Zhang, F., Chen, S., Chaturvedi, V., & Linhardt, R. J. (2020) · ACS Infectious Diseases · doi:10.1021/acsinfecdis.9b00450 · Cited by 47 · see citing works
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Cited by
Sorted by citations
Innate immune responses against the fungal pathogen Candida auris
Wang, Y., Zou, Y., Chen, X., Li, H., Yin, Z., Zhang, B., Xu, Y., Zhang, Y., Zhang, R., Huang, X., et al. (2022) · Nature Communications · doi:10.1038/s41467-022-31201-x · Cited by 107 · see citing works
Mechanisms of pathogenicity for the emerging fungus Candida auris
Horton, M. V., Holt, A. M., & Nett, J. E. (2023) · PLOS Pathogens · doi:10.1371/journal.ppat.1011843 · Cited by 67 · see citing works
Self-citationDatta, A., Das, D., Nett, J. E., Vyas, J. M., Lionakis, M. S., & Thangamani, S. (2023) · Microbiology Spectrum · doi:10.1128/spectrum.02215-23 · Cited by 30 · see citing works
Self-citationBalakumar, A., Das, D., Datta, A., Mishra, A., Bryak, G., Ganesh, S. M., Netea, M. G., Kumar, V., Lionakis, M. S., Arora, D., et al. (2024) · PLOS Pathogens · doi:10.1371/journal.ppat.1012699 · Cited by 25 · see citing works
Shivarathri, R., Chauhan, M., Datta, A., Das, D., Karuli, A., Aptekmann, A., Jenull, S., Kuchler, K., Thangamani, S., Chowdhary, A., et al. (2024) · mBio · doi:10.1128/mbio.02748-24 · Cited by 22 · see citing works
“The increased β-glucan in the cell wall mannosylation mutant strains has been shown to enhance neutrophil recruitment in a zebrafish infection model (63) and was associated with enhanced fungal killing by neutrophils and macrophages (62, 63).”
The Emerging Fungal Pathogen Candida auris Induces IFNγ to Colonize the Skin
Das, D., Ganesh, S. M., Mishra, A., Netea, M. G., & Thangamani, S. (2025) · PLOS Pathogens · doi:10.1371/journal.ppat.1013114 · Cited by 18 · see citing works
Yeast and filamentous <i>Candida auris</i> stimulate distinct immune responses in the skin
Bryak, G., Cox, A., Lionakis, M. S., & Thangamani, S. (2024) · mSphere · doi:10.1128/msphere.00055-24 · Cited by 13 · see citing works
“Furthermore, we predict that distinct skin immune responses observed between yeast and filamentous C. auris and C. albicans may in part due to the differences in the cell wall composition (24, 25).”
BackgroundBalakumar, A., Cox, A., & Thangamani, S. (2024) · mSphere · doi:10.1128/msphere.00734-24 · Cited by 12 · see citing works
Zarnowski, R., Horton, M. V., Johnson, C. J., Vang, P. C., Uram, J., Fernando, L. D. P., Vlach, J., Heiss, C., Azadi, P., Nett, J. E., et al. (2025) · mBio · doi:10.1128/mbio.00346-25 · Cited by 5 · see citing works
“However, neutrophils are less effective at engaging, phagocytosing, and killing C. auris when compared to C. albicans (21, 24).”
Self-citationHost–Candida auris interactions in the skin
Thangamani, S., Balakumar, A., Datta, A., Bryak, G., & Lionakis, M. S. (2026) · PLOS Pathogens · doi:10.1371/journal.ppat.1014075 · Cited by 3 · see citing works
Xie, J., Yan, L., Kadosh, D., & Xiong, N. (2026) · iScience · doi:10.1016/j.isci.2026.115862 · Cited by 1 · see citing works
- Authors
- Horton, M. V., Johnson, C. J., Zarnowski, R., Andes, B. D., Schoen, T. J., Kernien, J. F., Lowman, D., Kruppa, M. D., Ma, Z., Williams, D. L., Huttenlocher, A., & Nett, J. E.
- Affiliations
- University of Wisconsin–Madison (US)
- Department of Medicine, University of Wisconsin, Madison, Wisconsin, USA<?A3B2 show [zaq no="AQGRid1"]?>
- East Tennessee State University (US)
- Department of Medical Microbiology and Immunology, University of Wisconsin, Madison, Wisconsin, USA
- Corresponding author
- Nett, Jeniel E.
- ORCID
- Venue
- mSphere
- Publisher
- American Society for Microbiology
- Published
- 2021-06-30
- Volume
- 6
- Issue
- 3
- Pages
- e0040621-e0040621
- ISSN
- 2379-5042 (ISSN-L)
- PMC
- PMC8265655
- OpenAlex
- W3177114916
- Cited by
- 79
- References
- 3
- Citations by year
- 2026: 22 · 2025: 15 · 2024: 22 · 2023: 13 · 2022: 7
- FWCI
- 3.33
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- mSphere (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Commons - East Tennessee State University (East Tennessee State University) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Burroughs Wellcome Fund (1012299)
- Doris Duke Charitable Foundation (2017074)
- HHS | National Institutes of Health (R01AI145939, R21AI159583, R01GM083016, R01GM119197, R21AI15988, T32AI55397)
- 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, neutrophil phagocytosis, Candida albicans, Candida glabrata, fungal pathogenesis, drug resistance, invasive fungal infections
- MeSH terms
- Candida auris, Animals, Candida albicans, Cell Wall, Mannans, Neutrophils, Phagocytosis, Virulence, Zebrafish, Candida glabrata, Immune Evasion
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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