PERIPHERAL-BLOOD LYMPHOCYTE BETA-2 INTEGRIN AND ICAM EXPRESSION IN INFLAMMATORY BOWEL-DISEASE

The beta 2 integrin intercellular adhesion molecule (ICAM) adhesion pa thway is likely pivotal in the immunopathogenesis of inflammatory bowe l disease (IBD). We have undertaken a comprehensive study of periphera l 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 cortico steroids. Blood was collected from patients with Crohn's disease (N = 49), ulcerative colitis (N = 43), and normal control volunteers (N = 1 5). Mononuclear cells were separated using a Ficoll-Hypaque gradient a nd 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 a ctivity level, and for use of prednisone among patients with active di sease. There was decreased percentage expression of CD11a, CD18, and I CAM-3 in Crohn's disease and ulcerative colitis compared with normal, but an increased MFI for these molecules among patients with Crohn's d isease. Active Crohn's disease showed a greater change in this pattern compared with both inactive disease and active ulcerative colitis. CD 11a and CD18 histograms typically had two peaks of expression. The pre dominance 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 c hanges in the expression of beta 2 integrins in IBD, which were more e vident 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.