Candida tropicalis Alters Barrier Permeability and Claudin-1 Organization in Intestinal Epithelial Cells

Inflammatory bowel disease (IBD) is an autoimmune disorder characterized by chronic inflammation of the gut and compromised intestinal barrier function, resulting from aberrant immune responses targeting the intestinal microbiota. While the involvement of Candida albicans in IBD pathogenesis is well-documented, the role of non- albicans Candida species in IBD remains less understood. Recent studies have identified a correlation between elevated levels of Candida tropicalis , a notable non- albicans opportunistic fungus, and the development of IBD. However, the precise impact of C. tropicalis on intestinal barrier function is not well elucidated. To address this knowledge gap, we utilized a cell model comprising polarized Caco-2 monolayers, which mimic the intestinal epithelium, to investigate the interaction between C. tropicalis and intestinal barrier function. Our results showed that incubation with C. tropicalis influenced transepithelial electrical resistance and increased permeability to the small molecule lucifer yellow, but did not affect permeability to the larger molecule fluorescein isothiocyanate-dextran. In addition, we observed internalization of the tight junction protein claudin-1 in the Caco-2 monolayers. Further experiments using Caco-2 monolayers exposed to the dectin-1 ligand zymosan induced similar changes in the distribution of claudin-1 but did not alter monolayer permeability. These findings suggest that C. tropicalis specifically affects intestinal barrier integrity and permeability to smaller solutes in intestinal epithelial cells.