Intercellular adhesion molecule-1 (ICAM-1) in ulcerative colitis: presence, visualization, and significance.
The intensive research of recent years has suggested that the cause of ulcerative colitis (UC) involves a genetic predisposition to an uncontrolled or unbalanced immune response to luminal or epithelial antigens or against other external factors. Intercellular adhesion molecule-1 (ICAM-1) is pivotal for the influx of neutrophil granulocytes into colonic mucosa, and gene analyses have found polymorphisms in the gene encoding ICAM-1, indicating that changes in ICAM-1 function may be involved in the pathogenesis of UC. Clinical trials of the ICAM-1 antisense oligonucleotide Alicaforsen, which inhibits the synthesis of ICAM-1, have shown positive results in the treatment of patients with left-sided (distal) UC. In addition to emphasizing the central role of ICAM-1 in active stages of UC, the results provide hope for the development and introduction of a more specific and efficient treatment for UC than those currently available. This review discusses the results from studies on the expression of ICAM-1 in colonic tissue from patients with UC.
Vainer
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Department of Pathology, Rigshospitalet, University of Copenhagen, Denmark. ben.vainer@rh.hosp.dk
D000818:Animals; D000911:Antibodies, Monoclonal / Q000737:chemistry; D003093:Colitis, Ulcerative / Q000378:metabolism*; D003106:Colon / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology; D005786:Gene Expression Regulation; D006098:Granulocytes / Q000378:metabolism; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis* / Q000502:physiology*; D007413:Intestinal Mucosa / Q000473:pathology; D008214:Lymphocytes / Q000378:metabolism; D008854:Microscopy, Electron; D008954:Models, Biological; D009504:Neutrophils / Q000378:metabolism; D011110:Polymorphism, Genetic
D000911:Antibodies, Monoclonal; D018799:Intercellular Adhesion Molecule-1