Wound healing and fibrosis in intestinal disease

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Abstract
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. Available treatments of intestinal strictures, fibrosis and fistulas are insufficient and unsatisfactory. New therapeutic approaches are urgently needed. Future intervention should involve stronger and more selective prevention of the continuous tissue damage and a change in wound healing by modulation of myofibroblast migration and ECM synthesis.