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Inhibition of Proinflammatory Cytokine Expression by NF‐κB (p65) Antisense Oligonucleotide in Helicobacter pylori ‐Infected Mice
Author(s) -
Kim Sang Gyun,
Kim Joo Sung,
Kim Jung Mogg,
Chae Jung Hyun,
Sung Song In
Publication year - 2005
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/j.1523-5378.2005.00365.x
Subject(s) - proinflammatory cytokine , tumor necrosis factor alpha , gastric mucosa , helicobacter pylori , biology , interleukin , cytokine , microbiology and biotechnology , inflammation , immunology , stomach , biochemistry , genetics
Background. Helicobacter pylori induces the expression of proinflammatory cytokines in vitro by activating nuclear factor‐κB, a transcriptional regulator. However, it has not been clarified whether H. pylori ‐induced proinflammatory cytokines are also mediated through nuclear factor‐κB in vivo. The aim of this study was to evaluate the role of nuclear factor‐κB on the expressions of proinflammatory cytokines in H. pylori ‐infected mice. Materials and Methods. We evaluated nuclear factor‐κB (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‐κB pathway by using phosphorothioate antisense and sense oligonucleotide against the nuclear factor‐κB (p65). Results. In the H. pylori ‐infected gastric mucosa of mice, immunofluorescent staining using antip65 polyclonal antibody showed nuclear factor‐κB (p65) activation, which was particularly localized to epithelial cells. Tumor necrosis factor‐α and interleukin‐1β concentrations in gastric mucosa by enzyme‐linked immunosorbent assay (ELISA) were elevated in the infected group versus the uninfected group. Pretreatment with nuclear factor‐κB (p65) antisense oligonucleotide inhibited the activation of nuclear factor‐κB and the expressions of tumor necrosis factor‐α and interleukin‐1β 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‐κB in vivo, and this may play an important role in the initiation of H. pylori‐ induced gastric inflammation.