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The gastrointestinal (GI) microbiota acts a natural barrier to the proliferation of opportunistic pathogens.  Candida glabrata  is an opportunistic yeast pathogen that has adapted to colonize all segments of the human GI tract. We observed an increase in  Escherichia coli ,  Enterococcus faecalis , and  Bacteroides vulgatus  populations, and a decrease in  Lactobacillus johnsonii ,  Bacteroides thetaiotaomicron , and  Bifidobacterium animalis  in mice with DSS-induced colitis. This reduction was more pronounced for  L. johnsonii  during  C. glabrata  overgrowth. In addition,  C. glabrata  overgrowth increased mouse mortality and inflammatory parameters, and modulated the expression of intestinal receptors and signaling pathways. The  C. glabrata  cell wall underwent various changes during the course of  C. glabrata  colonization, and showed a significant increase in chitin.  C. glabrata  deficient in chitin synthase-3 induced fewer inflammatory parameters than the parental strain during intestinal inflammation. Oral administration of chitin attenuated the impact of colitis, and reduced the number of aerobic bacteria and  C. glabrata  overgrowth, while chitinase-3-like protein-1 increased. This study provides evidence that inflammation of the gut alters the microbial balance and leads to  C. glabrata  cell wall remodeling through an increase in chitin, which is involved in promoting persistence of  C. glabrata  in the gut.

Remodeling of the Candida glabrata cell wall in the gastrointestinal tract affects the gut microbiota and the immune response