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Nod2 mutation in Crohn's disease potentiates NF-kappaB activity and IL-1beta processing.

Science (New York, N.Y.) | Feb 4, 2005

Variants of NOD2, an intracellular sensor of bacteria-derived muramyl dipeptide (MDP), increase susceptibility to Crohn's disease (CD). These variants are thought to be defective in activation of nuclear factor kappaB (NF-kappaB) and antibacterial defenses, but CD clinical specimens display elevated NF-kappaB activity. To illuminate the pathophysiological function of NOD2, we introduced such a variant to the mouse Nod2 locus. Mutant mice exhibited elevated NF-kappaB activation in response to MDP and more efficient processing and secretion of the cytokine interleukin-1beta (IL-1beta). These effects are linked to increased susceptibility to bacterial-induced intestinal inflammation and identify NOD2 as a positive regulator of NF-kappaB activation and IL-1beta secretion.

Pubmed ID: 15692052 RIS Download

Mesh terms: Acetylmuramyl-Alanyl-Isoglutamine | Animals | Anti-Bacterial Agents | Apoptosis | Bacteria | Cells, Cultured | Colitis | Colon | Crohn Disease | Cytokines | Dextran Sulfate | Interleukin-1 | Intestinal Mucosa | Intracellular Signaling Peptides and Proteins | Lipopolysaccharides | Macrophage Activation | Macrophages | Mice | Mutation | NF-kappa B | Nod2 Signaling Adaptor Protein | Peptidoglycan | Signal Transduction

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Associated grants

  • Agency: NIAID NIH HHS, Id: AI43477
  • Agency: NIAID NIH HHS, Id: AI56075
  • Agency: NIDDK NIH HHS, Id: DK07202
  • Agency: NIDDK NIH HHS, Id: DK35108

Mouse Genome Informatics (Data, Gene Annotation)

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