Abstract
BackgroundThe intestinal mucous layer is a physical barrier that limits the contact between bacteria and host epithelial cells. There is growing evidence that microbiota-produced metabolites can also be specifically sensed by gut pathogens as signals to induce or repress virulence genes. Many E. coli, including adherent and invasive (AIEC) strains, can form biofilm. This property can promote their intestinal colonization and resistance to immune mechanisms. We sought to evaluate the impact of mucus-derived sugars on biofilm formation of E. coli.ResultsWe showed that the mucin sugar N-acetyl-glucosamine (NAG) can reduce biofilm formation of AIEC strain LF82. We demonstrated that the inactivation of the regulatory protein NagC, by addition of NAG or by mutation of nagC gene, reduced the biofilm formation of LF82 in static condition. Interestingly, real-time monitoring of biofilm formation of LF82 using microfluidic system showed that the mutation of nagC impairs the early process of biofilm development of LF82. Thus, NAG sensor NagC is involved in the early steps of biofilm formation of AIEC strain LF82 under both static and dynamic conditions. Its implication is partly due to the activation of type 1 fimbriae. NAG can also influence biofilm formation of other intestinal E. coli strains.ConclusionsThis study highlights how catabolism can be involved in biofilm formation of E. coli. Mucus-derived sugars can influence virulence properties of pathogenic E. coli and this study will help us better understand the mechanisms used to prevent colonization of the intestinal mucosa by pathogens.
Highlights
The intestinal mucous layer is a physical barrier that limits the contact between bacteria and host epi‐ thelial cells
We evaluated the influence of mucus-derived sugars on biofilm formation of Adherent-invasive E. coli (AIEC) reference strain LF82
We showed that mucus-derived sugars can influence biofilm formation of different E. coli strains from other pathotypes
Summary
The intestinal mucous layer is a physical barrier that limits the contact between bacteria and host epi‐ thelial cells. There is growing evidence that microbiota-produced metabolites can be sensed by gut pathogens as signals to induce or repress virulence genes. Many E. coli, including adherent and invasive (AIEC) strains, can form biofilm. This property can promote their intestinal colonization and resistance to immune mechanisms. Commensal E. coli colonize the large intestine in vertebrates and appear to reside inside the mucus layer without contacting the underlying epithelium [1]. The mucus layer that covers the intestinal epithelium plays a critical role in gut homeostasis. Several species of the gut microbiota release sugars from O-glycans into the intestinal lumen [7, 8]. Released mucus-derived sugars, including N-acetylglucosamine (NAG), N-acetylneuraminic acid (NANA), galactose, fucose, mannose and Sicard et al Gut Pathog (2018) 10:26
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