Interleukin-8 response of gastric epithelial cell lines to Helicobacter pylori stimulation in vitro
- 1 May 1995
- journal article
- Published by American Society for Microbiology in Infection and Immunity
- Vol. 63 (5), 1681-87
- https://doi.org/10.1128/iai.63.5.1681-1687.1995
Abstract
Gastric infection with Helicobacter pylori activates a mucosal inflammatory response by mononuclear cells and neutrophils that includes expression of cytokines interleukin-1 beta (IL-1 beta), IL-6, tumor necrosis factor alpha, and IL-8. In this study, we analyzed the IL-8 response of human gastric cancer cell lines (Kato III, AGS, and MKN28) to H. pylori infection in vitro. IL-8 mRNA expression was detected by reverse transcription-PCR amplification of RNA extracted from epithelial cells after incubation with different H. pylori wild-type and mutant strains, and IL-8 secretion was measured by an enzyme-linked immunosorbent assay. Exposure to viable H. pylori induced IL-8 mRNA and protein synthesis in all three gastric cell lines but not in nongastric epithelial cell lines. Heat-killed H. pylori and a crude cytotoxin preparation did not induce significant IL-8 secretion. IL-8 mRNA peaked between 2 and 4 h postinfection, and IL-8 protein production was maximal 24 h postinfection. Exposure of gastric carcinoma cells to other gastrointestinal bacteria, such as Pseudomonas aeruginosa, Campylobacter jejuni, and Escherichia coli, but not Campylobacter fetus, induced IL-8 synthesis. Wild-type strains that expressed the vacuolating cytotoxin (Tox+) and a cytotoxin-associated gene (cagA) product (CagA+) induced significantly more IL-8 than did CagA- Tox- strains. However, there was no decrease in IL-8 induction by isogenic mutants of CagA-, Tox-, or Cag- Tox- strains or by a mutant lacking the urease subunits. These results indicate that exposure to H. pylori and other gram-negative organisms that do not colonize the gastric mucosa induces IL-8 production by gastric carcinoma cells in vitro. Although the CagA+ Tox+ phenotype of H. pylori is associated with enhanced IL-8 production by gastric cell lines, other bacterial constituents are clearly essential.Keywords
This publication has 35 references indexed in Scilit:
- Expression of interleukin 8 and CD54 by human gastric epithelium after Helicobacter pylori infection in vitroGastroenterology, 1995
- Interleukin-8 expression in Helicobacter pylori infected, normal, and neoplastic gastroduodenal mucosa.Journal of Clinical Pathology, 1994
- Novel Pseudomonas product stimulates interleukin-8 production in airway epithelial cells in vitro.JCI Insight, 1994
- Attachment of Helicobacter pylori to Human Gastric Epithelium Mediated by Blood Group AntigensScience, 1993
- Review Of The Chemokine Meeting The Third International Symposium Of Chemotactic CytokinesCytokine, 1993
- Mucosal tumour necrosis factor alpha and interleukin-6 in patients with Helicobacter pylori associated gastritis.Gut, 1991
- Properties of the Novel Proinflammatory Supergene "Intercrine" Cytokine FamilyAnnual Review of Immunology, 1991
- Gastric Epithelial Cells in Helicobacter pylori‐Associated Gastritis Express HLA‐DR but not ICAM‐1Scandinavian Journal of Immunology, 1991
- Bacterial adhesion and Helicobacter pylori.Gut, 1991
- Prevalence of Helicobacter pylori Infection and Histologic Gastritis in Asymptomatic PersonsNew England Journal of Medicine, 1989