Comparative studies of the colonic in situ expression of intercellular adhesion molecules (ICAM-1,-2, and-3), beta(2) integrins (LFA-1, Mac-1, and p150,95), and PECAM-1 in ulcerative colitis and Crohn's disease

A dysregulated local immune defense with a constant influx of leukocytes pr ovides a basis for continuous intestinal inflammation in ulcerative colitis (UC) and Crohn's disease (CD). Cell adhesion molecules are pivotal for the migration of leukocytes from the circulation toward the colonic epithelium . A study quantifying the cells expressing; intercellular adhesion molecule s (ICAMs), beta(2) integrins, and platelet-endothelial cell adhesion molecu le-1 (PECAM-1) in the colon was performed to illustrate the leukocyte migra tion pathway in inflammatory bowel disease, Serial colonic sections (10 UC, 10 CD, and 10 controls) were stained immunohistochemically for ICAM-1, ICA M-2, ICAM-3, CD11a, CD11b, CD18, and PECAM-1. Cell adhesion molecule expres sion was evaluated quantitatively with reference to topographic localizatio n. In UC, poly morphonuclear leukocytes (PMNs) in contact with the crypt ep ithelium and in crypt abscesses expressed CD11b. CD tissue was characterize d by CD11a-, CD11c-, and ICAM-1-expressing cells. ICAM-1 was detected on en dothelial cells, leukocytes, and apical parts of epithelial membranes, wher eas ICAM-2 was expressed on basal epithelial membranes. Most infiltrating l eukocytes expressed ICAM-3, whereas perivascular mononuclear cells expresse d PECAM-1. Interestingly, the epithelial basement membrane in UC stained fo r CD18. In conclusion, CD11b, CD18, and ICAM-2 seem to be: important for PM N transepithelial migration in UC, whereas CD11a, CD11c, ICAM-1, and ICAM-3 seem central in leukocyte locomotion and aggregation in CD. Differentiated upregulation of cell adhesion molecules is suggested to be essential for t he diversities between UC and CD.