In vitro treatment with killed Helicobacter pylori downregulates the production of RANTES by PBMC.

The mechanisms by which Helicobacter pylori colonizes and persists within the gastric mucosa are poorly understood. The gastric immune response observed in vivo during H. pylori infection, is characterized by a polarization of Th1 cell type that seems to be responsible for gastric pathology. The purpose of this study was to test the direct effect of H. pylori cagA(+)/vacA(+ )(live and/or gentamicin-killed) on human peripheral blood mononuclear cells (PBMCs) in order to evaluate the production of regulated activation normal T cell expressed and secreted (RANTES) in vitro. We also evaluated the possible relationship between RANTES release and the presence of IL-12 and IFN-gamma in supernatants of the same cells. In the present study, we show for the first time that the low amount of RANTES in supernatants of PBMC incubated with killed H. pylori is linked, at least in part, to the inhibition of IL-12 and IFN-gamma release