Objectives: Despite H. pylori is known to be a sort of non-invasive bacteria, varying, degree of inflammatory reaction is observed in the gastric mucosa. Therefore, it is important to explore the mechanism of those inflammation for understanding
the
pathogenesis of H. pylori infection. We performed this study to test our hypothesis that H. pylori induced inflammation could be triggered by interlukin-8 (IL-8) expressed in human gastric epithelial cells in the early phase of H. pylori
infection
Methods: After human gastric epithelial cells, SNU-5 and KATOⅢ, were infected with H. pylori for 1, 4, and 9 hours, each RNAs were extracted from the gastric cells. And then IL-8 gene expression was assessed using RT-PCR and quantified by
standard
synthetic RNA. To determine cell affinity to H. pylori, IL-8 mRNA expression was explored not only in human gastric epithelial cells, SNU-5, KATOⅢ, AND Hs746T, but also in human ileocecal epithelial cells, HCT-8, and colonic epithelial cells,
HT-29
Results: IL-8 mRNA was expressed in SNU-5 and KATOⅢcells during entire infection period. In SNU-5, IL-8 mRNA was highly expressed (1.3×10E7 molecules/μg total RNA) at 1 hour and reached to peak level (1.0×10E3 molecules) at 9 hours. In
KATOⅢ,
IL-8
mRNA expression reached to peak level (1.5×10E8 molecules/μg total RNA) at 4 hours then decreased. Expression lovels of IL-8 mRNA were parallel to the amount of IL-8 protein measured by ELISA. IL-8 mRNA expression was not observed in
KATOⅢcells
infected with C. fetus subsp. fetus, C. jejuni, and E. coli DH5a. IL-8 mRNA expression was not only increased in gastric epithelial cells but also in non-gastric epithelial cells infected with H. pylori. Conclusion : Theses results suggest that
inflammatory reaction by H. pylori may be initially triggered by IL-8 expressed in infected gastric epithelial cells.
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