Abstract
Intestinal fungi are increasingly believed to greatly influence gut health. However, the effects of fungi on intestinal inflammation and on gut bacterial constitution are not clear. Here, based on pyrosequencing method, we reveal that fungal compositions vary in different intestinal segments (ileum, cecum, and colon), prefer different colonization locations (mucosa and feces), and are remarkably changed during intestinal inflammation in dextran sulfate sodium (DSS)-colitis mouse models compare to normal controls: Penicillium, Wickerhamomyces, Alternaria, and Candida are increased while Cryptococcus, Phialemonium, Wallemia and an unidentified Saccharomycetales genus are decreased in the guts of DSS-colitis mice. Fungi-depleted mice exhibited aggravated acute DSS-colitis associated with gain of Hallella, Barnesiella, Bacteroides, Alistipes, and Lactobacillus and loss of butyrate-producing Clostridium XIVa, and Anaerostipes compare with normal control. In contrast, bacteria-depleted mice show attenuated acute DSS-colitis. Mice with severely chronic recurrent DSS-colitis show increased plasma (1,3)-β-D-glucan level and fungal translocation into the colonic mucosa, mesenteric lymph nodes and spleen. This work demonstrate the different roles of fungi in acute and chronic recurrent colitis: They are important counterbalance to bacteria in maintaining intestinal micro-ecological homeostasis and health in acutely inflamed intestines, but can harmfully translocate into abnormal sites and could aggravate disease severity in chronic recurrent colitis.
Highlights
Fecal specimens, but the microbiota therein may not participate directly in disease initiation
We analyzed the fecal fungi in different GI segments with high-throughput sequencing and bioinformatics and demonstrated that the fungal compositions varied among GI segments and that fungal relative abundance showed an increased trend from ileum to colon
The fungal burden showed dichotomous behavior during intestinal inflammation: it increased in the mucosa but decreased in the feces, similar to observations for intestinal bacteria
Summary
Fecal specimens, but the microbiota therein may not participate directly in disease initiation. A genetic single-nucleotide polymorphism on Dectin-1, an immune cell receptor that recognizes β -glucan on the cell walls of various intestinal fungi, is usually associated with increased severity of ulcerative colitis in patients[3]. Ilieve et al.[3] reported that Dectin-1-deficient mice exhibit more severe experimental colitis accompanied by general expansion of opportunistic gut fungi and fungal invasion into the colonic mucosa. We investigated the fungal distribution in different segments (ileum, cecum, and colon) and locations (mucosa and feces) of the gut in normal and colitis mice, compared the roles of fungi and bacteria in intestinal inflammation, and studied the relationships between them to elucidate the function of fungi in intestinal inflammation and fungal-bacterial interactions in the GI canal. Our findings will be informative for future clinical IBD treatment
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