Abstract
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.
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.
| Original language | English |
|---|---|
| Pages (from-to) | 104-112 |
| Journal | Current Opinion in Microbiology |
| Volume | 40 |
| Early online date | 17 Nov 2017 |
| DOIs | |
| Publication status | E-pub ahead of print - 17 Nov 2017 |