Objectives:
@EN Despite the fact that H. pylori is known to be a sort of non-invasive bacteria, inflammatory reaction including mucosal infiltration of inflammtory cells has been 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 proinflammatory cytokines expressed in human gastric epithelial
cells
in the early phase of H. pylori infection.
@ES Methods:
@EN 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 proinflammatory cytokine gene expression was assessed using RT-PCR and
quantified by
standard synthetic RNA. Proinflammatory cytokines for this study were interleukin (IL)-1α, IL-1β, IL-6, IL-8, granulocyte macrophage colony stimulating factor (GM-CSF), monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factorα(TNFα)
and
RANTES (regulated on activation, normal T expressed and secreted).
@ES Results:
@EN IL-1α, IL-1βand IL-8 mRNA were expressed in SNU-5 and KATOⅢcells during entire infection period. In KATOⅢ, IL-1αand IL-8 mRNA expression reached to and reached to peak level at 9 hours. In KATOⅢ, IL-1αand IL-8 mRNA expression reached
to
peak
level at 4 hours and then decreased. IL-1βmRNA was expressed less than IL-1αor IL-8 mRNA. In SNU-5, GM-CSF, MCP-1 and TNFαmRNA were expressed at 9 hours, but in KATOⅢ, not expressed. IL-6 and RANTES mRNAs were not expressed in both SNU-5 and
KATOⅢ.
Expression levels of IL-8 mRNA were parallel to the amount of IL-8 protein measured by enzyme-linked immunosorbent assay (ELISA).
@ES Conclusion:
@EN These results suggest that inflammatory reaction by H, pylori may be initially triggered by proinflammatory cytokines expressed in infected gastric epithelial cells.
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