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G. Scott Lichtenberger, Richard A Flavell, Lena Alexopoulou, Innate Immunity and Apoptosis in IBD, Inflammatory Bowel Diseases, Volume 10, Issue suppl_1, 1 February 2004, Pages S58–S62, https://doi.org/10.1097/00054725-200402001-00012
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Extract
Ulcerative Colitis and Crohn's disease, collectively termed inflammatory bowel disease (IBD), are chronic inflammatory diseases of the gastrointestinal tract. The diseases are characterized by bloody diarrhea, abdominal pain, weight loss, fatigue, and increased risk of gastrointestinal malignancy. Understanding the molecular pathogenesis of IBD is critical toward developing new therapies. IBD appears to result from an inappropriate response to normal gastrointestinal flora. The normal mucosal immune system represents a balance between aggressive cells and regulatory cells that can suppress the activity of the former. This balance can be disturbed by either an enhanced effector cell response of the innate or adaptive immune system, or a deficiency of a regulatory mechanism. We will explore the role of innate immunity and apoptosis and how defects can lead to the imbalance seen in IBD.
TLRs in Mucosal Epithelium
Surface epithelium serves a critical function as the defensive front line of the mucosal innate immune system in the gastrointestinal tract. Initiation and perpetuation of the inflammatory intestinal responses in IBD may result from an exaggerated host defense reaction of the intestinal epithelium to microorganisms including species of commensal as well as pathogenic bacteria and viruses as well as food antigens present in the lumen. Recent studies have shown that mucosal epithelial cells 1,–3 and a wide variety of other cell types of the intestine such as intestinal macrophages of the lamina propria, 4 fetal intestinal cells, 5 gastric pit cells, 6 and intestinal myofibroblasts 7 express Toll like receptors (TLRs). These receptors evolved to detect the presence of infection through recognition of conserved pathogen associated molecular patterns and play an essential role in innate host defense as well as in the control of adaptive immune responses. 8,9
