Infection with Helicobacter pylori causes inflammation that can persist asymptomatically or evolve into more severe pathologies such as gastric or peptic ulcers, MALT lymphoma and gastric cancer. The cag pathogenicity island is one of the major virulence factors of this bacterium. Several cytokines and antimicrobial peptides are involved in modulating the inflammatory response of the gastric epithelial mucosa during infection with H. pylori. This work has focused on the study of the interactions between H. pylori and gastric epithelial cells. The in vivo study on a mouse model of infection described a profile of the antimicrobial response associated to this bacterium. Increased production of S100A9 may be involved in the failure of the bacteria implantation and colonization in the murine gastric mucosa. We have also established a new protocol for primary culture of human gastric epithelial cells from stomachs obtained after gastric sleeve interventions in subjects with morbid obesity. An infection model with H. pylori has also been established to study in vitro the inflammatory and antimicrobial responses of these cells after infection. The cag-dependent induction of a panel of inflammatory mediators and antimicrobial agents by gastric epithelial cells exposed to H. pylori confirms the involvement of this factor during the early inflammatory response. Gastric cells with stem cells phenotype were also isolated and phenotypic and molecular characterizations were initiated to determine their nature. The cell models developed in this study allow a better understanding of interactions between H. pylori and gastric epithelial cells.
