Candida Tropicalis Infection Dramatically Affects The Gut Microbiome In Dss-Induced Colitis

Abstract Candidiasis caused by Candida (C.) tropicalis has dramatically increased worldwide. The role of C. tropicalis in the pathogenesis of intestinal inflammation in Crohn’s disease patients has not been fully elucidated. We have previously reported that C57BL/6 mice infected with C. tropicalis show significantly increased severity of intestinal inflammation following induction of colitis by administration of dextran sodium sulfate (DSS) in drinking water. These effects were associated with increased gene expression of Tnfa and Ifng, and decreased expression of Th2-associated genes, such as Il4 and Il13. In the present study, we investigated the effects of C. tropicalis infection on the composition and function of the gut microbiome in this model. Analysis of 16s rRNA in fecal samples of infected mice showed that C. tropicalis significantly altered the gut microbiome composition, affecting, in particular, the abundance of mucin-degrading bacteria, such as Akkermansia Muciniphila and Ruminococcus Gnavus (β diversity analysis: P<.05). Alcian Blue staining showed a significant decrease of mucus-producing goblet cells in infected mice before and after DSS-induced colitis (number of goblet cells per power field: 50.3±9.1 vs. 21.4±5.4; P<.05). Flow cytometry analysis showed that in lymph nodes of infected mice, there was a higher percentage of group 2 innate lymphoid cells (% ILC2: 10.28±2.28 vs. 2.08±0.34, P<.05). Our data demonstrate that C. tropicalis may play a pro-inflammatory role in intestinal injury by altering the gut microbiome community and affecting the abundance of specific mucin-degrading bacteria. Therefore, the resulting dysbiosis may affect the susceptibility of the host to develop inflammatory bowel disease.