Candida albicans–epithelial interactions and induction of mucosal innate immunity

•Candidalysin is the first peptide toxin identified in any human fungal pathogen.•Epithelial cells identify invasive C. albicans by detecting Candidalysin activity.•Neutrophils are critical for protection against mucosal C. albicans infection.•IL-17 signaling is essential for immunity to mucosal C....

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Bibliographic Details
Published in:Current opinion in microbiology 2017-12, Vol.40, p.104-112
Main Authors: Naglik, Julian R, König, Annika, Hube, Bernhard, Gaffen, Sarah L
Format: Article
Language:English
Subjects:
Animals
Candida albicans - genetics
Candida albicans - physiology
Candidiasis - genetics
Candidiasis - immunology
Candidiasis - microbiology
Epithelial Cells - immunology
Epithelial Cells - microbiology
Humans
Immunity, Innate
Mucous Membrane - immunology
Mucous Membrane - microbiology
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Summary:•Candidalysin is the first peptide toxin identified in any human fungal pathogen.•Epithelial cells identify invasive C. albicans by detecting Candidalysin activity.•Neutrophils are critical for protection against mucosal C. albicans infection.•IL-17 signaling is essential for immunity to mucosal C. albicans infections.•Candidalysin induces innate Type 17 production via IL-1 receptor signaling. Candida albicans is a human fungal pathogen that causes millions of mucosal and life-threatening infections annually. C. albicans initially interacts with epithelial cells, resulting in fungal recognition and the formation of hyphae. Hypha formation is critical for host cell damage and immune activation, which are both driven by the secretion of Candidalysin, a recently discovered peptide toxin. Epithelial activation leads to the production of inflammatory mediators that recruit innate immune cells including neutrophils, macrophages and innate Type 17 cells, which together work with epithelial cells to clear the fungal infection. This review will focus on the recent discoveries that have advanced our understanding of C. albicans-epithelial interactions and the induction of mucosal innate immunity.
ISSN:1369-5274
1879-0364
DOI:10.1016/j.mib.2017.10.030