title: Activation of nuclear factor kappa B inflammatory bowel disease.
abstract: BACKGROUND
  Expression of pro-inflammatory cytokines is increased in the intestinal lamina propria of patients with inflammatory bowel disease (IBD). Nuclear factor kappa B (NF kappa B) controls transcription of inflammation genes. On activation, NF kappa B is rapidly released from its cytoplasmic inhibitor (I kappa B), transmigrates into the nucleus, and binds to DNA response elements in gene promoter regions.
  
  
  OBJECTIVE
  To investigate whether increased activation of NF kappa B is important in IBD and may be down-regulated by anti-inflammatory treatment.
  
  
  METHODS
  Activation of NF kappa B was determined by western blot assessment and electrophoretic mobility shift assay in nuclear extracts of colonic biopsy samples as well as lamina propria mononuclear cells.
  
  
  RESULTS
  Nuclear levels of NF kappa B p65 are increased in lamina propria biopsy specimens from patients with Crohn's disease in comparison with patients with ulcerative colitis and controls. Increased activation of NF kappa B was detected in lamina propria mononuclear cells from patients with active IBD. Corticosteroids strongly inhibit intestinal NF kappa B activation in IBD in vivo and in vitro by stabilising the cytosolic inhibitor I kappa B alpha against activation induced degradation.
  
  
  CONCLUSIONS
  In both IBDs, but particularly Crohn's disease, increased activation of NF kappa B may be involved in the regulation of the inflammatory response. Inhibition of NF kappa B activation may represent a mechanism by which steroids exert an anti-inflammatory effect in IBD.
authors.affiliation: Charité University Hospital, 4th Medical Department, Humboldt University, Berlin, Germany.
authors.forename: S
authors.initials: S
authors.lastname: Schreiber
authors.forename: S
authors.initials: S
authors.lastname: Nikolaus
authors.forename: J
authors.initials: J
authors.lastname: Hampe
mesh_terms: D000293:Adolescent; D000328:Adult; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001623:Betamethasone / Q000627:therapeutic use; D015153:Blotting, Western; D003093:Colitis, Ulcerative / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism; D003106:Colon / Q000737:chemistry / Q000378:metabolism*; D003424:Crohn Disease / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000032:analysis / Q000378:metabolism; D005260:Female; D006801:Humans; D020672:I-kappa B Proteins; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000032:analysis / Q000037:antagonists & inhibitors / Q000378:metabolism*; D011239:Prednisolone / Q000627:therapeutic use; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D000893:Anti-Inflammatory Agents; D004268:DNA-Binding Proteins; D020672:I-kappa B Proteins; D016328:NF-kappa B; C000606204:NFKBIA protein, human; D000072000:NF-KappaB Inhibitor alpha; D001623:Betamethasone; D011239:Prednisolone