Alterations in mucosa branched <i>N</i>-glycans lead to dysbiosis and downregulation of ILC3: a key driver of intestinal inflammation.

ABSTRACT: The perturbation of the symbiotic relationship between microbes and intestinal immune system contributes to gut inflammation and Inflammatory Bowel Disease (IBD) development. The host mucosa glycans (glycocalyx) creates a major biological interface between gut microorganisms and host immunity that remains ill-defined. Glycans are essential players in IBD immunopathogenesis, even years before disease onset. However, how changes in mucosa glycosylation shape microbiome and how this impact gut immune response and inflammation remains to be clarified. Here, we revealed that alterations in the expression of complex branched N-glycans at gut mucosa surface, modeled in glycoengineered mice, resulted in dysbiosis, with a deficiency in Firmicutes bacteria. Concomitantly, this mucosa N

SUBMITTER: Rodrigues CS 

PROVIDER: S-EPMC11810091 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature