Modulation and adherence of intestinal mucus by commensal bacteria and the pathogen C. difficile

Abstract

Gut pathogens initially encounter the host at the gastrointestinal (GI) mucus layer making its regulation a crucial aspect of gut health. Few studies have addressed bacteria‐mucus adherence or mucus oligosaccharide utilization by commensal or pathogenic bacteria. To address this gap in knowledge, the interaction between mucus (human stool, HT‐29‐MTX cells and human ileal enteroids) and commensal bacteria (B. thetaiotaomicron, C. coccoides, C. butryicum, B. producta, A. muciniphila, F. prausnitzii, R. torques, L. reuteri) or the pathogen C. difficile was examined. In vitro cultures in tryptone‐yeast extract media revealed that C. difficile and B. producta were capable of using multiple types of oligosaccharides (fucose, mannose, galactose, GlcNAc, GalNAC, sialic acid) as a sole carbon source, while other commensal bacteria exhibited specific oligosaccharide preferences. Commensal bacteria had enhanced adherence to mucus from human stool compared to HT‐29‐MTX mucus. Additionally, FITC‐labeled oligosaccharide specific lectins demonstrated that all tested commensal bacteria were capable of altering mucus oligosaccharide composition. Select commensal species were also able to stimulate mucus secretion. In contrast, the pathogen C. difficile adhered to multiple oligosaccharides in human stool mucus, but had limited adherence to HT‐29‐MTX mucus. C. difficile did not stimulate mucus secretion in HT‐29‐MTX cells and decreased secretion in enteroids. Together this data demonstrates that commensal and pathogenic bacteria adhere directly to GI mucus, but this interaction is mucin type and composition dependent. Manipulation or adherence to intestinal mucus may represent a method of bacterial‐host modulation. T32DK07644