Neutrophils Do Not Express IL-17A in the Context of Acute Oropharyngeal Candidiasis

IL-17 protects against pathogens by acting on nonhematopoietic cells to induce neutrophil recruitment through upregulation of chemokines and G-CSF. IL-17- and Th17-deficient humans and mice are susceptible to mucosal Candida albicans infections, linked to impaired neutrophil responses. IL-17 product...

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Bibliographic Details
Published in:Pathogens (Basel) 2015-07, Vol.4 (3), p.559-572
Main Authors: Huppler, Anna R, Verma, Akash H, Conti, Heather R, Gaffen, Sarah L
Format: Article
Language:English
Subjects:
Acquired immune deficiency syndrome
AIDS
Brief Report
Candida albicans
Chemokines
Cytokines
Flow cytometry
fungal infection
HIV
Human immunodeficiency virus
IL-17
Infections
innate lymphocyte
Lymphocytes
mice
Neutrophils
oral candidiasis
Pathogens
Pediatrics
TCR
Th17
γδ-T cell
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Summary:IL-17 protects against pathogens by acting on nonhematopoietic cells to induce neutrophil recruitment through upregulation of chemokines and G-CSF. IL-17- and Th17-deficient humans and mice are susceptible to mucosal Candida albicans infections, linked to impaired neutrophil responses. IL-17 production is traditionally associated with CD4+ Th17 cells. However, IL-17 is also expressed during innate responses to facilitate rapid pathogen clearance. Innate IL-17-expressing cells include various lymphocyte-type subsets, including ILC3, NKT, γδ-T and "natural" Th17 (nTh17) cells. Some reports suggest that neutrophils can express IL-17 during fungal infections. Here, we asked whether neutrophils serve as a source of IL-17 during acute oropharyngeal candidiasis (OPC) using an IL-17A fate-tracking reporter mouse. Mice were subjected to OPC for two days, and oral tissue was analyzed by flow cytometry. IL-17A was expressed by γδ-T cells and TCRβ+ natural Th17 (nTh17) cells, as recently reported. Although infiltrating neutrophils were recruited to the tongue following infection, they did not express the IL-17A reporter. Moreover, neutrophil-depleted mice exhibited normal transcription of both Il17a and downstream IL-17-dependent gene targets after Candida challenge. Thus, in acute OPC, neutrophils are not a measurable source of IL-17 production, nor are they necessary to trigger IL-17-dependent gene expression, although they are essential for ultimate pathogen control.
ISSN:2076-0817
2076-0817
DOI:10.3390/pathogens4030559