title: Peripheral blood lymphocyte beta 2 integrin and ICAM expression in inflammatory bowel disease.
abstract: The beta 2 integrin intercellular adhesion molecule (ICAM) adhesion pathway is likely pivotal in the immunopathogenesis of inflammatory bowel disease (IBD). We have undertaken a comprehensive study of peripheral blood lymphocyte (PBL) expression of all beta 2 integrins and ICAMs in patients with IBD using flow cytometry and assessed our data on the basis of IBD diagnosis, disease state of activity, and use of corticosteroids. Blood was collected from patients with Crohn's disease (N = 49), ulcerative colitis (N = 43), and normal control volunteers (N = 15). Mononuclear cells were separated using a Ficoll-Hypaque gradient and prepared for flow cytometry. The data were analyzed for percentage expression, mean fluorescent intensity (MFI) as well as for histogram patterns. The analysis was stratified for disease diagnosis, disease activity level, and for use of prednisone among patients with active disease. There was decreased percentage expression of CD11a, CD18, and ICAM-3 in Crohn's disease and ulcerative colitis compared with normal, but an increased MFI for these molecules among patients with Crohn's disease. Active Crohn's disease showed a greater change in this pattern compared with both inactive disease and active ulcerative colitis. CD11a and CD18 histograms typically had two peaks of expression. The predominance of one peak over the other varied with disease diagnosis and activity. CD11b and alpha d expression patterns were not different in IBD compared with normal. CD11c was not expressed by PBLs and, ICAM-2, typically an endothelial ligand, was expressed on PBLs. There were changes in the expression of beta 2 integrins in IBD, which were more evident in Crohn's disease than ulcerative colitis. We hypothesize that the decreased percentage expression and increased MFI of CD11a, CD18, and ICAM-3 may suggest that cells up-regulate these ligands following activation and are egressing into tissue.
authors.affiliation: Department of Internal Medicine, University of Manitoba, Winnipeg, Canada.
authors.forename: C N
authors.initials: CN
authors.lastname: Bernstein
authors.forename: M
authors.initials: M
authors.lastname: Sargent
authors.forename: P
authors.initials: P
authors.lastname: Rawsthorne
authors.forename: E
authors.initials: E
authors.lastname: Rector
mesh_terms: D000328:Adult; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D015703:Antigens, CD; D000943:Antigens, Differentiation; D018845:CD11 Antigens / Q000032:analysis; D018821:CD18 Antigens / Q000032:analysis; D015815:Cell Adhesion Molecules / Q000097:blood*; D003093:Colitis, Ulcerative / Q000097:blood*; D003424:Crohn Disease / Q000097:blood* / Q000188:drug therapy; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D016023:Integrins / Q000097:blood; D008297:Male; D011239:Prednisolone / Q000627:therapeutic use; D011446:Prospective Studies; D015854:Up-Regulation
chemical_list: D000893:Anti-Inflammatory Agents; D015703:Antigens, CD; D000943:Antigens, Differentiation; D018845:CD11 Antigens; D018821:CD18 Antigens; D015815:Cell Adhesion Molecules; C483616:ICAM3 protein, human; D016023:Integrins; D011239:Prednisolone