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Inhibition of proinflammatory cytokine expression by NF-kappaB (p65) antisense oligonucleotide in Helicobacter pylori-infected mice
Cited 13 time in
Web of Science
Cited 14 time in Scopus
- Authors
- Issue Date
- 2005-11-24
- Publisher
- Wiley-Blackwell
- Citation
- Helicobacter. 2005 Dec;10(6):559-66.
- Keywords
- 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
- Abstract
- 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.
- ISSN
- 1083-4389 (Print)
- Language
- English
- URI
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16302981
https://hdl.handle.net/10371/22865
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