Abstract

RECENT ADVANCES IN BASIC SCIENCE WOUNDHEALINGANDFIBROSISIN INTESTINAL DISEASE F Rieder, J Brenmoehl, S Leeb, J Scho ¨lmerich, G Rogler Gut 2007; 56:130–139. doi: 10.1136/gut.2006.090456 he mechanisms of wound healing in general have gained interest in recent years, as it has become obvious that the tightly regulated process of tissue repair and regeneration is of great T importance for organ homeostasis. Insufficient as well as excessive tissue repair both impair gastrointestinal function. Formation of ulcers and fistulas on the one hand, and of fibrosis and stricture on the other, represent just two sides of one medal. So far, the physiological pathways involved in intestinal wound healing are only partially understood. During acute and chronic intestinal inflammation, macrophages and neutrophils induce local tissue damage by secreting reactive oxygen radicals and tissue-degrading enzymes. This is followed by the release of pro-inflammatory cytokines, as well as chemotactic and cell-activating peptides previously bound to the matrix. If tissue damage is severe, myofibroblasts migrate to the sites of the defect. This migratory function, the ability to contract the wound area and the production of extracellular matrix (ECM) by intestinal myofibroblast cells certainly have important roles in the physiological situation and are altered by chronic inflammation.