Epithelial glycosylation in gut homeostasis and inflammation.

Abstract

Intestinal epithelial cells apically express glycans, especially α1,2-fucosyl linkages, which work as a biological interface for the host-microbe interaction. Emerging studies have shown that epithelial α1,2-fucosylation is regulated by microbes and by group 3 innate lymphoid cells (ILC3s). Dysregulation of the gene (FUT2) encoding fucosyltransferase 2, an enzyme governing epithelial α1,2-fucosylation, is associated with various human disorders, including infection and chronic inflammatory diseases. This suggests a critical role for an interaction between microbes, epithelial cells and ILC3s mediated via glycan residues. In this Review, using α1,2-fucose and Fut2 gene expression as an example, we describe how epithelial glycosylation is controlled by immune cells and luminal microbes. We also address the pathophysiological contribution of epithelial α1,2-fucosylation to pathogenic and commensal microbes as well as the potential of α1,2-fucose and its regulatory pathway as previously unexploited targets in the development of new therapeutic approaches for human diseases.

• Authors: Yoshiyuki Goto, Satoshi Uematsu, Hiroshi Kiyono
• Journal: Nature immunology (Nat Immunol) Vol. 17 Issue 11 Pg. 1244-1251 (Oct 19 2016) ISSN: 1529-2916 [Electronic] United States
• PMID: 27760104 (Publication Type: Journal Article, Review)

Chemical References

• Carbohydrates
• Fucose
• Fucosyltransferases
• galactoside 2-alpha-L-fucosyltransferase

Topics

• Animals
• Carbohydrate Metabolism
• Carbohydrates
• Fucose (metabolism)
• Fucosyltransferases (genetics, metabolism)
• Gastroenteritis (genetics, immunology, metabolism, microbiology)
• Genetic Predisposition to Disease
• Glycosylation
• Homeostasis
• Host-Pathogen Interactions (immunology)
• Humans
• Immunity, Innate
• Immunity, Mucosal
• Intestinal Mucosa (immunology, metabolism, microbiology)
• Lymphocytes (immunology, metabolism)
• Polymorphism, Genetic