Candida pathogens induce protective mitochondria-associated type I interferon signalling and a damage-driven response in vaginal epithelial cells.

摘要: Vaginal candidiasis is an extremely common disease predominantly caused by four phylogenetically diverse species: Candida albicans; glabrata; parapsilosis; and tropicalis. Using a time course infection model of vaginal epithelial cells dual RNA sequencing, we show that these species exhibit distinct pathogenicity patterns, which are defined highly species-specific transcriptional profiles during cells. In contrast, host homogeneous response to all at the early stages infection, characterized sublethal mitochondrial signalling inducing protective type I interferon response. At later stages, diverges in species-dependent manner. This divergence primarily driven extent damage elicited mechanisms, such as secretion toxin candidalysin C. albicans. Our results uncover dynamic, biphasic species, mitochondria-associated damage-driven