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Inflammatory Bowel Disease (IBD)
IBD, which affects approximately 1 in 500 of the population, is a generic term that includes Crohn’s diseae (CD) and ulcerative colitis (UC). However, some very significant differences in the inflammatory response in these two conditions seem to reflect the underlying mechanisms of the two diseases. Recently we have shown major abnormalities in the inflammatory response to bacteria in these two conditions1, 2, 3. Whereas, UC is characterised by prolonged inflammation due to a defective resolution phase, CD results from impaired acute inflammation (review4). Macrophages are grossly abnormal in these two conditions and play a central role in disease progression. We are currently investigating the precise mechanisms that fail in CD and UC. In CD it appears to involve the secretory machinery required for pro-inflammatory cytokine release. In UC the problem appears to involve a signaling system that switches on the production and release of resolving mediators. Acute inflammation is normally only switched on for about 24 hours. This suppression does not occur, or is delayed, in UC. We are currently investigating the signaling pathways normally activated in macrophages by bacteria and then determine where they are defective in UC cells. These approaches should greatly increase our knowledge of these two chronic inflammatory diseases and facilitate the development of rational treatment.
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