Cutting edge: The IkappaB kinase (IKK) inhibitor, NEMO-binding domain peptide, blocks inflammatory injury in murine colitis

J Immunol. 2007 Sep 1;179(5):2681-5. doi: 10.4049/jimmunol.179.5.2681.

Abstract

Inflammatory mediators such as TNF-alpha, IL-6, and IL-1 are important in the pathogenesis of inflammatory bowel diseases and are regulated by the activation of NF-kappaB. The aim of the present study was to investigate whether the NF-kappaB essential modulator (NEMO)-binding domain (NBD) peptide, which has been shown to block the association of NEMO with the IkappaB kinasebeta subunit (IKKbeta) and inhibit NF-kappaB activity, reduces inflammatory injury in mice with colitis. Two colitis models were established by the following: 1) inclusion of dextran sulfate sodium salt (DSS) in the drinking water of the mice; and 2) a trinitrobenzene sulfonic acid enema. Marked NF-kappaB activation and expression of proinflammatory cytokines were observed in colonic tissues. The NBD peptide ameliorated colonic inflammatory injury through the down-regulation of proinflammatory cytokines mediated by NF-kappaB inhibition in both models. These results indicate that an IKKbeta-targeted NF-kappaB blockade using the NBD peptide could be an attractive therapeutic approach for inflammatory bowel disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Colitis / chemically induced
  • Colitis / drug therapy*
  • Colitis / pathology
  • Cytokines / antagonists & inhibitors
  • Cytokines / metabolism
  • Dextran Sulfate / toxicity
  • Disease Models, Animal
  • I-kappa B Kinase / antagonists & inhibitors*
  • Lipopolysaccharides / immunology
  • Mice
  • Mice, Inbred C57BL
  • NF-kappa B / antagonists & inhibitors
  • Peptides / therapeutic use*
  • Trinitrobenzenesulfonic Acid / toxicity

Substances

  • Cytokines
  • Lipopolysaccharides
  • NBD peptide, mouse
  • NF-kappa B
  • Peptides
  • Trinitrobenzenesulfonic Acid
  • Dextran Sulfate
  • I-kappa B Kinase