| Proinflammatory Pathways are Down-regulated by NF- |
| Helicobacter pylori에 감염된 마우스에서 NF-κB (p65) Antisense Oligonucleotide에 의한 친염증성 반응 경로의 억제 |
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김상균·김주성·김정목*·정현채·송인성 |
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서울대학교 의과대학 내과학교실, 간연구소, 한양대학교 의과대학 미생물학교실, 의과학연구소* |
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| Abstract |
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Background/Aims: Helicobacter pylori (H. pylori) induces the expression of proinflammatory cytokines in vitro by activating nuclear factor-κB (NF-κB). However, it has not been clarified whether H. pylori-induced proinflammatory cytokines are also mediated through NF-κB in vivo. We conducted this study to evaluate the role of NF-κB on the expressions of proinflammatory cytokines in H. pylori-infected mice. Methods: We evaluated NF-κB (p65) activation in the H. pylori-infected gastric mucosa of mice by immunofluorescent staining using anti-p65 polyclonal antibody, and the expressions of proinflammatory cytokines with inhibition of NF-κB pathway by using phosphorothioate antisense oligonucleotide (AS-ODN) against NF-κB (p65). Results: In the H. pylori-infected gastric mucosa, immunofluorescent staining using anti-p65 antibody showed NF-κB (p65) activation, which was particularly localized to epithelial cells. Tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) concentrations in gastric mucosa by enzyme-linked immunosorbent assay (ELISA) were elevated in the infected group versus the uninfected group. Pretreatment with NF-κB (p65) AS-ODN inhibited the activation of NF-κB and the expressions of TNF-α and IL-1β in H. pylori-infected gastric mucosa. Conclusions: H. pylori infection was found to activate the expressions of proinflammatory cytokines via NF-κB in vivo, and this may play an important role in the initiation of H. pylori-induced gastric inflammation. (The Korean Journal of Helicobacter and Upper Gastrointestinal Research 2005;5:134-142) |
| Key Words:
Helicobacter pylori, Nuclear factor-κB, Antisense oligonucleotide, Tumor necrosis factor-α, Interleukin-1β |
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