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Cited by 112Antifungal resistance and susceptibilityNeutrophil, Myeloperoxidase and Oxidative MechanismsFungal and yeast genetics research

IL-1 Coordinates the Neutrophil Response to C. albicans in the Oral Mucosa

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Altmeier, Simon, Toska, Albulena, Sparber, Florian, Teijeira, Alvaro, Halin, Cornelia, LeibundGut-Landmann, Salomé·2016·PLOS Pathogens
DOI 10.1371/journal.ppat.1005882PMC PMC5025078
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Abstract

Mucosal infections with Candida albicans belong to the most frequent forms of fungal diseases. Host protection is conferred by cellular immunity; however, the induction of antifungal immunity is not well understood. Using a mouse model of oropharyngeal candidiasis (OPC) we show that interleukin-1 receptor (IL-1R) signaling is critical for fungal control at the onset of infection through its impact on neutrophils at two levels. We demonstrate that both the recruitment of circulating neutrophils to the site of infection and the mobilization of newly generated neutrophils from the bone marrow depended on IL-1R. Consistently, IL-1R-deficient mice displayed impaired chemokine production at the site of infection and defective secretion of granulocyte colony-stimulating factor (G-CSF) in the circulation in response to C. albicans. Strikingly, endothelial cells were identified as the primary cellular source of G-CSF during OPC, which responded to IL-1α that was released from keratinocytes in the infected tissue. The IL-1-dependent crosstalk between two different cellular subsets of the nonhematopoietic compartment was confirmed in vitro using a novel murine tongue-derived keratinocyte cell line and an established endothelial cell line. These data establish a new link between IL-1 and granulopoiesis in the context of fungal infection. Together, we identified two complementary mechanisms coordinating the neutrophil response in the oral mucosa, which is critical for preventing fungal growth and dissemination, and thus protects the host from disease.

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  • IL-1R signaling is critical for neutrophil function.

    “IL-1R signaling is critical for neutrophil function [26, 31, 32]”

    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 [31]

    The Results section on neutrophil recruitment (page unavailable) says IL-1R signaling was critical for the neutrophil response during oropharyngeal candidiasis in mice. The Discussion (page unavailable) specifies that the demonstrated effects concern neutrophil recruitment and production; it does not establish that IL-1R signaling is critical for neutrophil function generally or for neutrophils’ intrinsic activity. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • IL-1R signaling is critical for neutrophil recruitment and function and plays an important role in host defense against C. albicans in oral mucosa and systemic infection.

    “IL-1R signaling is critical for neutrophil recruitment and function and plays an important role in the host defense against C. albicans in oral mucosa and systemic infection [31, 32]”

    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 [31]

    The Results and Discussion show that IL-1R signaling promotes neutrophil recruitment and fungal control in a mouse model of oral candidiasis. The Discussion also reports previous evidence for an IL-1R role in systemic candidiasis, but this paper does not establish that IL-1R regulates neutrophil function during systemic infection; it says the protective mechanism was not addressed in most of those studies. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

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Cited by

Sorted by citations

Authors
Altmeier, S., Toska, A., Sparber, F., Teijeira, A., Halin, C., & LeibundGut-Landmann, S.
Affiliations
  • University of Zurich (CH)
  • ETH Zurich (CH)
ORCID
Venue
PLOS Pathogens
Publisher
Public Library of Science (PLoS)
Published
2016-09-15
Volume
12
Issue
9
Pages
e1005882
ISSN
  • 1553-7366 (ISSN-L)
  • 1553-7374
DOI
10.1371/journal.ppat.1005882
PMC
PMC5025078
OpenAlex
W2519902791
Cited by
112
References
6
Citations by year
2026: 5 · 2025: 7 · 2024: 10 · 2023: 6 · 2022: 13 · 2021: 12 · 2020: 18 · 2019: 10 · 2018: 19 · 2017: 11
FWCI
12.31
Type
journal article
Language
en
Open access
Licence
Locations
  • PLoS Pathogens (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
  • Figshare (submittedVersion, cc-by)
  • Repository for Publications and Research Data (ETH Zurich) (submittedVersion, cc-by)
  • Zurich Open Repository and Archive (University of Zurich) (submittedVersion, cc-by)
  • ETH Zürich Research Collection (cc-by)
  • Zurich Open Repository and Archive (University of Zurich)
Funders
  • Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (PP00P3_150758, CRSII3_141848)
  • Austrian Science Fund (J3566)
Topics
  • Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
Keywords
interleukin-1 receptor signaling, Candida albicans, oropharyngeal candidiasis, neutrophils, neutrophil recruitment, granulopoiesis, granulocyte colony-stimulating factor, endothelial cells, keratinocytes, chemokine production, antifungal immunity, oral mucosa, host defense against fungi
MeSH terms
Animals, Candida albicans, Candidiasis, Mouth Mucosa, Neutrophils, Tongue, Keratinocytes, Granulocyte Colony-Stimulating Factor, Receptors, Interleukin-1, Mice, Knockout, Myelopoiesis, Endothelial Cells, Mice, Interleukin-1alpha

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