Cytokine - Intestinal Epithelial Cell Interactions: Implications for Immune Mediated Bowel Disorders

The intestinal epithelial cell population is comprised of a dynamic continuum, ranging from undifferentiated, actively proliferating crypt cells, to mature absorptive villus enterocytes, lacking mitotic capacity. Under normal conditions, the constant loss of differentiated villus tip cells via apoptosis leads to a complete renewal of the epithelial cell population every few days. The physiological factors regulating enterocyte proliferation, maturation and apoptosis in health, as well as those that modulate these events in disease states remain largely unknown. It has been demonstrated in vitro that immature crypt cell proliferation is stimulated by factors such as TGF α and TNF a, whereas TGF β and IFN γ inhibit mitotic activity. Further studies showed that intestinal epithelial cells are able to produce and secrete several cytokines such as 1L6, 1L8, TNF a, TGF α and TGF β, indicating the potential for autocrine and paracrine responses. A variety of immune mediated bowel disorders, including celiac disease, Crohn’s disease and ulcerative colitis, are characterized by accelerated epithelial cell turnover and apoptosis, leading to altered crypt/villus morphology. There is increasing evidence that these changes, and the accompanying functional alterations of the bowel epithelium, are mediated by the cytokines released from infiltrating inflammatory cells, as well as from enterocytes themselves in an autocrine fashion.

並列關鍵字

cytokines ； intestinal epithelial cell ； proliferation ； apoptosis ； inflammatory bowel disorders

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