Candida albicans releases a peptide from the Rbt1 protein to promote its invasion into the gut epithelium.

Candida albicans has been recently added to the WHO critical priority group of fungal pathogens based on its impact on global public health. C. albicans is a mucosal commensal yeast in humans that can cause severe gastro-intestinal-borne disseminated candidiasis in immunocompromised patients. C. albicans interaction with enterocytes is thus a key step in the pathophysiology of disseminated candidiasis. Here, we show that, during the first steps of the infection process, C. albicans releases a peptide from the Repressed by Tup1 protein 1 (Rbt1) that disorganizes the cell-cell adhesion junctions in Caco-2 intestinal epithelial cells, by notably downregulating constitutive proteins of the tight junction complex (i.e. ZO-1). This is the first report to show that a peptide of a human pathogenic fungus promotes fungal invasion into the gut epithelium by disorganizing the protective epithelial barrier.