RETRACTED: Activation of intercellular adhesion molecule 1 expression by Helicobacter pylori is regulated by NF-κB in gastric epithelial cancer cells (Retracted article. See vol. 79, pg. 542, 2011)

Interactions between leukocytes and epithelial cells may play a key role in Helicobacter pylori-associated gastric mucosal inflammation. This process is mediated by various cell adhesion molecules. The present study examined the molecular mechanisms leading to H. pylori-induced epithelial cell intercellular adhesion molecule-1 (ICAM-1; also called CD54) expression. Coculture of epithelial cells dth cytotoxin-associated gene pathogenicity island-positive (cag PAI(+)) H. pylori strains, but not with a cag PAI(-) strain or H. pylori culture supernatants, resulted in upregulation of steady-state mRNA levels and cell surface expression of ICAM-1. Coculture with H. pylori induced an increase in luciferase activity in cells which were transfected with a luciferase reporter gene linked to the 5'-flanking region of the ICAM-1 gene. H. pylori activated the ICAM-1 promoter via the NF-kappa B binding site. An inducible nuclear protein complex bound to the ICAM-1 NF-kappa B site and was identified as the NF-kappa B p50-p65 heterodimer, H. pylori induced the degradation of I kappa B-alpha, a major cytoplasmic inhibitor of NF-kappa B, and stimulated the expression of I kappa B-alpha mRNA Pretreatment of epithelial cells with pyrrolidine dithiocarbamate, which blocks NF-kappa B activation, inhibited RT, pylori-induced ICAM-1 expression. THP-1 macrophagic cells, peripheral blood mononuclear cells, and purified neutrophils adhered to RI. pylori-infected epithelial cells to a greater extent than to uninfected cells. These results show that H. pylori directly induces expression of ICAM-1 on gastric epithelial cells in an NF-kappa B-dependent manner that may support leukocyte attachment during inflammation.