H. pylori receptor MHC class II contributes to the dynamic gastric epithelial apoptotic response.

Aim: To investigate the role of MHC class II in the modulation of gastric epithelial cell apoptosis induced by H pylori infection.

Methods: After stimulating a human gastric epithelial cell line with bacteria or agonist antibodies specific for MHC class II and CD95, the quantitation of apoptotic and anti-apoptotic events, including caspase activation, BCL-2 activation, and FADD recruitment, was performed with a fluorometric assay, a cytometric bead array, and confocal microscopy, respectively.

Results: Pretreatment of N87 cells with the anti-MHC class II IgM antibody RFD1 resulted in a reduction in global caspase activation at 24 h of H pylori infection.

H pylori receptor MHC class II contributes to the dynamic gastric epithelial apoptotic response.

Aim: To investigate the role of MHC class II in the modulation of gastric epithelial cell apoptosis induced by H pylori infection.

Methods: After stimulating a human gastric epithelial cell line with bacteria or agonist antibodies specific for MHC class II and CD95, the quantitation of apoptotic and anti-apoptotic events, including caspase activation, BCL-2 activation, and FADD recruitment, was performed with a fluorometric assay, a cytometric bead array, and confocal microscopy, respectively.

Results: Pretreatment of N87 cells with the anti-MHC class II IgM antibody RFD1 resulted in a reduction in global caspase activation at 24 h of H pylori infection.

Helicobacter pylori binds to CD74 on gastric epithelial cells and stimulates interleukin-8 production.

The pathogenesis associated with Helicobacter pylori infection requires consistent contact with the gastric epithelium. Although several cell surface receptors have been suggested to play a role in adhesion, the bacterium-host interactions that elicit host responses are not well defined. This study investigated the interaction of H.