Abstract
Recent research into the role of the nuclear receptor protein PRR-γ in controlling imflammatory responses to the gut microflora might provide a molecular target for a diagnostic tool distinguishing ulcerative colitis (UC) from Crohn's disease. PRR-γ is known to counteract inflammation by blocking the NF-κB-mediated activation of transcription of inflammatory genes. The protein is present in phagocytic macrophages and colon cells. Sven Pettersson and co-workers from the Karolinska Insitute in Stockholm, Sweden report that exposing colon cells to LPS and peptidoglycan causes PRR-γ to bind to and inhibit NF-κB. Furthermore, patients with UC have lower levels of PRR-γ in the gut epithelium than normal, healthy individuals, suggesting that a defect in the mechanisms that switch off inflammation might be responsible for the disease. By contrast, patients with Crohn's disease, which is often confused with UC, have normal levels of PRR-γ. This finding suggests that different mechanisms are responsible for the two diseases. Drugs used to increase the activity of PRR-γ in type II diabetes patients might have potential therapeutic value in UC, but not Crohn's disease, patients. KM
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