Helicobacter pylori outer membrane vesicles modulate proliferation and interleukin-8 production by gastric epithelial cells.
Helicobacter pylori infection, which is always associated with gastritis, can progress to ulceration or malignancy. The diversity in clinical outcomes is partly attributed to the expression of virulence factors and adhesins by H. pylori. However, H. pylori may not have to adhere to the epithelium to cause gastritis. We hypothesize that outer membrane vesicles (OMV), which are constantly shed from the surface of H. pylori, play a role as independent activators of host cell responses. In this study, we found that low doses of OMV from cag PAI+ toxigenic and cag PAI- nontoxigenic strains increased proliferation of AGS gastric epithelial cells. At higher doses, we detected growth arrest, increased toxicity, and interleukin-8 (IL-8) production. The only strain differences detected were vacuolation with the toxigenic strain and higher levels of IL-8 production with OMV from the cag PAI- nontoxigenic strain. In summary, we suggest that constitutively shed OMV play a role in promoting the low-grade gastritis associated with H. pylori infection.
D002455:Cell Division; D002460:Cell Line; D002462:Cell Membrane / Q000276:immunology; D004847:Epithelial Cells / Q000276:immunology / Q000473:pathology; D005756:Gastritis / Q000209:etiology / Q000276:immunology / Q000473:pathology; D016481:Helicobacter Infections / Q000209:etiology / Q000276:immunology / Q000473:pathology; D016480:Helicobacter pylori / Q000276:immunology / Q000472:pathogenicity*; D006801:Humans; D016209:Interleukin-8 / Q000096:biosynthesis*; D013270:Stomach / Q000276:immunology / Q000473:pathology; D014774:Virulence
D016209:Interleukin-8