![]() ![]() These data indicate that ARG2 deletion results in compensatory upregulation of gastric polyamine synthesis and catabolism during H. Gastric tissues from infected Arg2 −/− mice demonstrated increased expression of arginase 1, ornithine decarboxylase, adenosylmethionine decarboxylase 1, spermidine/spermine N 1-acetyltransferase 1, and spermine oxidase, along with increased spermine levels. There was an increased expression of the Th1/ Th17 cytokines, interferon gamma and interleukin 17, in gastric tissues and splenic T-cells from Arg2 −/−, but not Nos2 −/− or Arg2 −/− Nos2 −/− mice. While Arg2 −/− mice demonstrated enhanced M1 macrophage activation, Nos2 −/− and Arg2 −/− Nos2 −/− mice did not demonstrate these changes, but exhibited increased CXCL1 and CXCL2 responses. Compared to wild-type mice, both Arg2 −/− and Arg2 −/− Nos2 −/− mice exhibited increased gastritis and decreased colonization, the latter indicating that the effect of ARG2 deletion on bacterial burden was not mediated by NO. We now bred Arg2 −/− to Nos2 −/− mice, and infected them with H. Our studies implicated a potential role for inducible nitric oxide (NO) synthase (NOS2), as Arg2 −/− mice exhibited increased NOS2 levels in gastric macrophages, and NO can kill H. We reported that arginase 2 (ARG2) deletion results in increased gastritis and decreased bacterial burden during Helicobacter pylori infection in mice. ![]()
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