BACKGROUND: Helicobacter pylori induces the expression of proinflammatory cytokines in vitro by activating nuclear factor-kappaB, a transcriptional regulator. However, it has not been clarified whether H. pylori-induced proinflammatory cytokines are also mediated through nuclear factor-kappaB in vivo. The aim of this study was to evaluate the role of nuclear factor-kappaB on the expressions of proinflammatory cytokines in H. pylori-infected mice. MATERIALS AND METHODS: We evaluated nuclear factor-kappaB (p65) activation in the H. pylori-infected gastric mucosa of mice by immunofluorescent staining using antip65 polyclonal antibody, and the expressions of proinflammatory cytokines with inhibition of nuclear factor-kappaB pathway by using phosphorothioate antisense and sense oligonucleotide against the nuclear factor-kappaB (p65). RESULTS: In the H. pylori-infected gastric mucosa of mice, immunofluorescent staining using antip65 polyclonal antibody showed nuclear factor-kappaB (p65) activation, which was particularly localized to epithelial cells. Tumor necrosis factor-alpha and interleukin-1beta concentrations in gastric mucosa by enzyme-linked immunosorbent assay (ELISA) were elevated in the infected group versus the uninfected group. Pretreatment with nuclear factor-kappaB (p65) antisense oligonucleotide inhibited the activation of nuclear factor-kappaB and the expressions of tumor necrosis factor-alpha and interleukin-1beta in H. pylori-infected gastric mucosa. Sense oligonucleotide did not influence on the expression of proinflammatory cytokines. CONCLUSIONS: H. pylori infection was found to activate the expressions of proinflammatory cytokines via nuclear factor-kappaB in vivo, and this may play an important role in the initiation of H. pylori-induced gastric inflammation.
BACKGROUND:Helicobacter pylori induces the expression of proinflammatory cytokines in vitro by activating nuclear factor-kappaB, a transcriptional regulator. However, it has not been clarified whether H. pylori-induced proinflammatory cytokines are also mediated through nuclear factor-kappaB in vivo. The aim of this study was to evaluate the role of nuclear factor-kappaB on the expressions of proinflammatory cytokines in H. pylori-infected mice. MATERIALS AND METHODS: We evaluated nuclear factor-kappaB (p65) activation in the H. pylori-infected gastric mucosa of mice by immunofluorescent staining using antip65 polyclonal antibody, and the expressions of proinflammatory cytokines with inhibition of nuclear factor-kappaB pathway by using phosphorothioate antisense and sense oligonucleotide against the nuclear factor-kappaB (p65). RESULTS: In the H. pylori-infected gastric mucosa of mice, immunofluorescent staining using antip65 polyclonal antibody showed nuclear factor-kappaB (p65) activation, which was particularly localized to epithelial cells. Tumor necrosis factor-alpha and interleukin-1beta concentrations in gastric mucosa by enzyme-linked immunosorbent assay (ELISA) were elevated in the infected group versus the uninfected group. Pretreatment with nuclear factor-kappaB (p65) antisense oligonucleotide inhibited the activation of nuclear factor-kappaB and the expressions of tumor necrosis factor-alpha and interleukin-1beta in H. pylori-infected gastric mucosa. Sense oligonucleotide did not influence on the expression of proinflammatory cytokines. CONCLUSIONS:H. pyloriinfection was found to activate the expressions of proinflammatory cytokines via nuclear factor-kappaB in vivo, and this may play an important role in the initiation of H. pylori-induced gastric inflammation.