S-Space College of Medicine/School of Medicine (의과대학/대학원) Internal Medicine (내과학전공) Journal Papers (저널논문_내과학전공)
Inhibition of proinflammatory cytokine expression by NF-kappaB (p65) antisense oligonucleotide in Helicobacter pylori-infected mice
- Kim, Sang Gyun; Kim, Joo Sung; Kim, Jung Mogg; Chae, Jung Hyun; Sung, Song In
- Issue Date
- Helicobacter. 2005 Dec;10(6):559-66.
- Animals; Cytokines/*antagonists & inhibitors/metabolism; Female; Gastric Mucosa/drug effects/*immunology/microbiology/physiopathology; Helicobacter Infections/*drug therapy/immunology/physiopathology; Helicobacter pylori/*immunology/pathogenicity; Interleukin-1/antagonists & inhibitors/metabolism; Mice; Mice, Inbred C57BL; Oligonucleotides, Antisense/administration &; dosage/*pharmacology/therapeutic use; Transcription Factor RelA/*antagonists & inhibitors/metabolism; Tumor Necrosis Factor-alpha/antagonists & inhibitors/metabolism
- 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.
- 1083-4389 (Print)
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