EXPRESSION OF INTERLEUKIN-8 AND CD54 BY HUMAN GASTRIC EPITHELIUM AFTER HELICOBACTER-PYLORI INFECTION IN-VITRO

Background/Aims: Helicobacter pylori is associated with neutrophil inf iltrates, although the mechanism of their recruitment is only partiall y defined. The aim of the study was to determine if Kato III, a human gastric epithelial cell line, expressed cytokines and the intercellula r adhesion molecule 1 (ICAM-1), which could contribute to the initiati on of inflammation during infection with H. pylori. Methods: Kato III cells were stimulated with H. pylori and were examined for evidence of infection, cytokine production, and the expression of ICAM-1. Results : The expression of interleukin 8 messenger RNA and immunoreactive pro tein by Kato III cells was significantly increased over constitutive l evels within 3 hours of infection with H. pylori. Infected Kato III su pernatants activated neutrophils as evidenced by increased CD11b/CD18 and decreased L-selectin that could be blocked by anti-interleukin 8. In contrast, Campylobacter jejuni, lipopolysaccharide, killed H. pylor i, and supernatants from cultures of H. pylori did not increase interl eukin 8. Interleukins 2 and 6; interferons alfa, beta, and gamma; and tumor necrosis factor were not produced by resting or H. pylori-stimul ated Kato III cells. In addition to producing interleukin 8, Kato III constitutively expressed surface ICAM-1, which acts as an intercellula r adhesion molecule for neutrophils. Conclusions: Our results indicate that H. pylori stimulates the gastric epithelium to initiate inflamma tion and neutrophil recruitment and activation.