Inflammation of the gut alters the microbial balance and leads to Candida glabrata cell wall remodeling

S. Jawhara1, Y. Pruvost2, G. Tumba2, F. Istel3, D. Poulain2 , K. Kuchler3, B. Sendid2, R. Charlet4

Author address: 

1LIRIC-INSERM 995/Team2, LILLE, France 2LIRIC-Inserm U995/Team2, LILLE, France 3Medical University Vienna, VIENNA, Austria 4LIRIC-Inserm 995/Team2, LILLE, France


Objective: The gastrointestinal microbiota acts a natural barrier to colonization and proliferation of opportunistic pathogens, thereby decreasing the risk of intestinal infection and disease. Deregulation of the dynamic crosstalk between the microbiota, intestinal epithelial cells and immune cells is critically involved in the development of inflammatory bowel disease. Experimental studies have shown that either Candida albicans or Candida glabrata aggravate intestinal inflammation induced by dextran sulfate sodium (DSS) in mice, and, conversely, that DSS colitis promotes fungal colonization. C. glabrata is an opportunistic yeast pathogen that has adapted to colonize all segments of the human GI tract. Methods: In the present study, we investigated the impact of C. glabrata colonization on the diversity of the gut microbiota in a DSS-induced colitis model, and assessed how the C. glabrata cell wall is remodeled in order to persist in the gut environment. We also analyzed the effect of chitin deficiency on C. glabrata-host interactions in the DSS mouse model. Results: We observed an increase in Escherichia coli, Enterococcus faecalis, and Bacteroides vulgatis 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. Conclusion: 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.


abstract No: 


Full conference title: 

20th Congress of the International Society for Human and Animal Mycology, Amsterdam, the Netherlands
    • ISHAM 20th (2018)