| Literature DB >> 15351034 |
Suguru Hasegawa1, Shinsuke Nishikawa, Tomisato Miura, Yoshihiko Saito, Hiroo Madarame, Kenji Sekikawa, Yoh-Ichi Tagawa, Yoichiro Iwakura, Akio Nakane.
Abstract
Helicobacter pylori colonizes the gastric mucosa of human and causes chronic gastritis. The previous studies have demonstrated that gamma interferon (IFN-gamma) but not tumor necrosis factor-alpha (TNF-alpha) plays a critical role in pathogenesis of gastritis induced by H. pylori infection. In this study we investigated the induction of gastritis induced by H. felis infection in TNF-alpha-deficient mice, comparing with IFN-gamma-deficient mice. The scores of gastritis and epithelial changes of TNF-alpha-deficient mice and IFN-gamma-deficient mice were significantly lower than that of C57BL/6 mice. Moreover, the degrees of gastritis and epithelial changes of TNF-alpha-deficient mice were rather low compared with that of IFN-gamma-deficient mice. In spleen cell cultures stimulated with heat-killed H. felis, IFN-gamma production by TNF-alpha-deficient mice and TNF-alpha production by IFN-gamma-deficient mice were significantly reduced compared with those in C57BL/6 mice. These results suggested that TNF-alpha is involved in pathogenesis of gastritis induced by H. felis infection as IFN-gamma and that an interaction between TNF-alpha and IFN-gamma might be required in pathogenesis of gastritis induced by Helicobacter infection.Entities:
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Year: 2004 PMID： 15351034 DOI： 10.1016/j.micpath.2004.06.004
Source DB: PubMed Journal: Microb Pathog ISSN： 0882-4010 Impact factor: 3.738