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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
Kim, Sang Gyun; Kim, Joo Sung; Kim, Jung Mogg; Chae, Jung Hyun; Sung, Song In
Issue Date
2005-11-24
Publisher
Wiley-Blackwell
Citation
Helicobacter. 2005 Dec;10(6):559-66.
Keywords
AnimalsCytokines/*antagonists & inhibitors/metabolismFemaleGastric Mucosa/drug effects/*immunology/microbiology/physiopathologyHelicobacter Infections/*drug therapy/immunology/physiopathologyHelicobacter pylori/*immunology/pathogenicityInterleukin-1/antagonists & inhibitors/metabolismMiceMice, Inbred C57BLOligonucleotides, Antisense/administration &dosage/*pharmacology/therapeutic useTranscription Factor RelA/*antagonists & inhibitors/metabolismTumor 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

http://hdl.handle.net/10371/22865
DOI
https://doi.org/10.1111/j.1523-5378.2005.00365.x
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College of Medicine/School of Medicine (의과대학/대학원)Internal Medicine (내과학전공)Journal Papers (저널논문_내과학전공)
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