1. ¹Laboratoire d'Anatomie-Pathologique, Faculté de Médecine, Nice, France
2. ²INSERM 452, Faculté de Médecine, Nice, France
3. ³INSERM 364, Faculté de Médecine, Nice, France
4. ⁴INSERM 526, Faculté de Médecine, Nice, France

Correspondence: Dr. Paul Hofman, INSERM Unité 364, Faculté de Médecine, avenue de Valombrose, 06107 Nice, Cédex 02, France. E-mail: hofman@unice.fr

Received 13 November 2000.

Abstract

A prominent histologic feature of Helicobacter pylori infection is a dense infiltration of polymorphonuclear leukocytes (PMNL) in gastric mucosa. H. pylori lipopolysaccharide (LPS) has been recognized as a primary virulence factor evoking acute mucosal inflammatory reaction. Previous works have shown that H. pylori LPS immunologic activities are lower than those of enterobacterial LPS. However, the effect of H. pylori LPS on spontaneous PMNL apoptosis, and mechanisms by which this H. pylori LPS may promote PMNL survival remain to be established. In this study, we investigated, by both morphologic and biochemical approaches, the action of H. pylori LPS on PMNL apoptosis 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 VacA, cag pathogenicity island and urease status. We demonstrated that LPS in BCF is responsible for this effect because it was abrogated by the LPS antagonist B287 (a synthetic analog of Rhodobacter sphaeroides lipid A). Moreover, BCF from H. pylori induced P42/44^{MAP kinase} activation in PMNL. Similar results were obtained with BCF of an Escherichia coli strain. Taken together these data suggest that longer survival of PMNL induced by H. pylori LPS may increase gastric epithelium injury in H. pylori–associated diseases.