The <i>Candida albicans</i> toxin candidalysin mediates distinct epithelial inflammatory responses through p38 and EGFR-ERK pathways.

ABSTRACT: The fungal pathogen Candida albicans secretes the peptide toxin candidalysin, which damages epithelial cells and drives an innate inflammatory response mediated by the epidermal growth factor receptor (EGFR) and mitogen-activated protein kinase (MAPK) pathways and the transcription factor c-Fos. In cultured oral epithelial cells, candidalysin activated the MAPK p38, which resulted in heat shock protein 27 (Hsp27) activation, IL-6 release, and EGFR phosphorylation without affecting the induction of c-Fos. p38 activation was not triggered by EGFR but by two nonredundant pathways involving MAPK kinases (MKKs) and the kinase Src, which differentially controlled p38 signaling outputs. Whereas MKKs mainly promoted p38-dependent release of IL-6, Src promoted p38-mediated phosphorylation of

SUBMITTER: Nikou SA 

PROVIDER: S-EPMC7612652 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature