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An emerging new paradigm suggests that changes in the homeostasis of bacteria\u2010 and host\u2010derived signal transduction at the epithelial cell level may lead to functional and immune disturbances of the intestinal epithelium. It has become clear from numerous studies that enteric bacteria are a critical component in the development and prevention\/treatment of chronic intestinal inflammation. Signal\u2010specific activation of mitogen\u2010activated protein kinases (MAPK), interferon\u2010regulated factors (IRF) and the transcription factor NF\u2010\u03baB through pattern recognition receptor signalling effectively induce inflammatory defence mechanisms. Unbalanced activation of these innate signalling pathways because of host genetic predispositions and\/or the lack of adequate anti\u2010inflammatory feedback mechanisms may turn a physiological response into a pathological situation including failure of bacterial clearance and development of chronic inflammation. Host\u2010derived regulators from the immune and enteric nerve system crosstalk to the innate signalling network of the intestinal epithelium in order to shape the extent and duration of inflammatory processes.<\/jats:p>","DOI":"10.1111\/j.1365-2982.2006.00762.x","type":"journal-article","created":{"date-parts":[[2006,2,16]],"date-time":"2006-02-16T15:21:48Z","timestamp":1140103308000},"page":"184-199","source":"Crossref","is-referenced-by-count":34,"title":["Intestinal epithelial cell signalling and host\u2010derived negative regulators under chronic inflammation: to be or not to be activated determines the balance towards commensal 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