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The Korean Journal of Helicobacter  and Upper Gastrointestinal Research 2001;1(1):9-13.
Published online December 30, 2001.
Role of Cytokine in H. pylori-Induced Gastric Mucosal Inflammation
Helicobacter pylori 감염에 의한 위점막 염증반응에서의 Cytokine의 역할
정현채
서울대학교 의과대학 내과학교실, 간연구소
Abstract
Despite the fact that Helicobacter pylori is known to be non-invasive, mucosal infiltration of inflammatory cells has been observed in the gastric mucosa. The exact pathogenesis of such an inflammatory reaction has not been well defined. After gastric epithelial cells, SNU-5 and KATO III, were infected with H. pylori, IL(interleukin)-8, IL-1α and IL-1β mRNAs were expressed in both gastric epithelial cells throughout the entire infection period. In SNU-5 cells, GM(granulocyte macrophage)-CSF(colony stimulating factor), MCP(monocyte chemoattractant protein)-1 and TNF(tumor necrosis factor)-α mRNAs were expressed at 9 hours. Gene expression paralleled the amount of IL-8 protein measured by ELISA. IL-8 mRNA expression was not observed in KATO III cells infected with C. fetus subsp. fetus, C. jejuni or E. coli. These results suggest that an inflammatory reaction induced by H. pylori may be initially triggered by an array of proinflammatory cytokines expressed by infected gastric epithelial cells. Chemokine expression could be found in gastric mucosa of patients infected with H. pylori. GROα and ENA-78 mRNA transcripts in H. pylori-infected gastric mucosa showed 14- and 15- fold increase, as compared with non-infected mucosa. Activation of neutrophis and upregulation of CXC chemokines such as IL-8 and GROs in neutrophils by H. pylori water extract could be observed in vitro. H. pylori-induced neutrophil recruitment may be mediated by such CXC chemokines. (Korean J Helicobacter Res Prac 2001;1:9-13)
Key Words: Chemokine, Gastric epithelial cells, Helicobacter pylori, Neutrophil, Proinflammatory cytokines


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