Helicobacter pylori induces β3GnT5 in human gastric cell lines, modulating expression of the SabA ligand sialyl–Lewis x

• DOI: 10.1172/jci34324
• Publication Date: 2008-05-15T20:13:55Z
• Authors: Nuno T. Marcos; Ana Magalhães; Bibiana Ferreira; Maria J. Oliveira; Ana S. Carvalho; Nuno Mendes; Tim Gilmartin; Steven R. Head; Céu Figueiredo; Leonor David; Filipe Santos-Silva; Celso A. Reis
• Keywords: CagA; Sialyl-Lewis X; Pathogenicity island

Chronic Helicobacter pylori infection is recognized as a cause of gastric cancer. H. adhesion to cells mediated by bacterial adhesins such sialic acid–binding adhesin (SabA), which binds the carbohydrate structure sialyl–Lewis x. Sialyl–Lewis x expression in epithelium induced during persistent infection, suggesting that modulates host cell glycosylation patterns for enhanced adhesion. Here, we evaluate changes glycosylation-related gene profile human carcinoma line following infection. We observed significantly altered 168 1,031 genes tested microarray, and extent these alterations was associated with pathogenicity strain. A highly pathogenic strain several involved glycan biosynthesis, particular encoding β3 GlcNAc T5 (β3GnT5), transferase essential biosynthesis Lewis antigens. β3GnT5 induction specific strains carrying cluster known cag island, dependent on CagA CagE. Further, overexpression lines led increased This study identifies what believe be novel mechanism SabA ligand cells, thereby strengthening epithelial attachment necessary achieve successful colonization.