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Review article: In vitro models in inflammatory bowel disease research--a critical review
D M McKay1, D J Philpott, M H Perdue
1Intestinal Disease Research Programme, McMaster University, Hamilton, Ontario, Canada.
Research efforts in inflammatory bowel disease (IBD) have been directed towards the epithelium as it has become clear that epithelial cells play a critical role in inflammatory response. Most research involving IBD employs in vitro techniques. In vitro epithelial cell studies have played and are continuing to play a major role in providing specific information relevant to IBD. Thus, such studies have provided irrefutable evidence that epithelial responses can be induced by microbes/microbial products and by immune activation. Culture experiments have provided insights into the effects of individual cytokines and other inflammatory mediators on epithelial pathophysiology, injury and repair, apoptosis, necrosis, and other processes that may be involved in IBD. Activated epithelial cells can participate in and even orchestrate immune responses, by stimulating T cells (and possibly others) and by producing cytokines that recruit specific inflammatory cells. Physiological regulation of epithelial tight junctions has been demonstrated by in vitro studies; the implication of this information for treating IBD is just beginning to be explored. It is becoming increasingly clear that epithelial processing and presentation of antigens is critical to the outcome of the immune response.
Research efforts in inflammatory bowel disease (IBD) have been directed towards the epithelium as it has become clear that epithelial cells play a critical role in inflammatory response. Most research involving IBD employs in vitro techniques. In vitro epithelial cell studies have played and are continuing to play a major role in providing specific information relevant to IBD. Thus, such studies have provided irrefutable evidence that epithelial responses can be induced by microbes/microbial products and by immune activation. Culture experiments have provided insights into the effects of individual cytokines and other inflammatory mediators on epithelial pathophysiology, injury and repair, apoptosis, necrosis, and other processes that may be involved in IBD. Activated epithelial cells can participate in and even orchestrate immune responses, by stimulating T cells (and possibly others) and by producing cytokines that recruit specific inflammatory cells. Physiological regulation of epithelial tight junctions has been demonstrated by in vitro studies; the implication of this information for treating IBD is just beginning to be explored. It is becoming increasingly clear that epithelial processing and presentation of antigens is critical to the outcome of the immune response.