Helicobacter pylori lipopolysaccharide hinders polymorphonuclear leucocyteapoptosis

A prominent histologic feature of Helicobacter pylori infection is a dense infiltration of polymorphonuclear leukocytes (PMNL) in gastric mucosa. H. p ylori lipopolysaccharide (LPS) has been recognized as a primary virulence f actor evoking acute mucosal inflammatory reaction. Previous works have show n that H. pylori LPS immunologic activities are lower than those of enterob acterial LPS. However, the effect of H. pylori LPS on spontaneous PMNL apop tosis, and mechanisms by which this H. pylori LPS may promote PMNL survival remain to be established. in this study, we investigated, by both morpholo gic and biochemical approaches, the action of H. pylori LPS on PMNL apoptos is in vitro, using broth culture filtrates (BCF) of H. pylori strains with different genotypes. We found that BCF from H. pylori caused a significant delay in spontaneous PMNL apoptosis and this delay was independent of the V acA, cag pathogenicity island and urease status. We demonstrated that LPS i n BCF is responsible for this effect because it was abrogated by the LPS an tagonist B287 (a synthetic analog of Rhodobacter sphaeroides lipid A). More over. BCF from H. pylori induced p42/44(MAP kinase) activation in PMNL. Sim ilar results were obtained with BCF of an Escherichia coil strain. Taken to gether these data suggest that longer survival of PMNL induced by H. pylori LPS may increase gastric epithelium injury in H. pylori-associated disease s.