Tumor necrosis factor-α is required for gastritis induced by Helicobacter felis infection in mice
Helicobacter pylori colonizes the gastric mucosa of human and causes chronic gastritis. The previous studies have demonstrated that gamma interferon (IFN-Î³) but not tumor necrosis factor-Î± (TNF-Î±) 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-Î±-deficient mice, comparing with IFN-Î³-deficient mice. The scores of gastritis and epithelial changes of TNF-Î±-deficient mice and IFN-Î³-deficient mice were significantly lower than that of C57BL/6 mice. Moreover, the degrees of gastritis and epithelial changes of TNF-Î±-deficient mice were rather low compared with that of IFN-Î³-deficient mice. In spleen cell cultures stimulated with heat-killed H. felis, IFN-Î³ production by TNF-Î±-deficient mice and TNF-Î± production by IFN-Î³-deficient mice were significantly reduced compared with those in C57BL/6 mice. These results suggested that TNF-Î± is involved in pathogenesis of gastritis induced by H. felis infection as IFN-Î³ and that an interaction between TNF-Î± and IFN-Î³ might be required in pathogenesis of gastritis induced by Helicobacter infection.