Peripheral Blood Lymphocyte β2 Integrin and ICAM Expression in Inflammatory Bowel Disease

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Abstract
The β2 integrin intercellular adhesionmolecule (ICAM) adhesion pathway is likely pivotal inthe immunopathogenesis of inflammatory bowel disease(IBD). We have undertaken a comprehensive study ofperipheral blood lymphocyte (PBL) expression of allβ2 integrins and ICAMs in patients with IBD usingflow cytometry and assessed our data on the basis of IBDdiagnosis, disease state of activity, and use ofcorticosteroids. Blood was collected from patients with Crohn'sdisease (N = 49), ulcerative colitis (N = 43), andnormal control volunteers (N = 15). Mononuclear cellswere separated using a Ficoll-Hypaque gradient and prepared for flow cytometry. The data wereanalyzed for percentage expression, mean fluorescentintensity (MFI) as well as for histogram patterns. Theanalysis was stratified for disease diagnosis, disease activity level, and for use of prednisone amongpatients with active disease. There was decreasedpercentage expression of CD11a, CD18, and ICAM-3 inCrohn's disease and ulcerative colitis compared with normal, but an increased MFI for thesemolecules among patients with Crohn's disease. ActiveCrohn's disease showed a greater change in this patterncompared with both inactive disease and activeulcerative colitis. CD11a and CD18 histograms typicallyhad two peaks of expression. The predominance of onepeak over the other varied with disease diagnosis andactivity. CD11b and alphad expression patterns were not different in IBD compared with normal.CD11c was not expressed by PBLs and, ICAM-2, typicallyan endothelial ligand, was expressed on PBLs. There werechanges in the expression of β2 integrins in IBD, which were more evident in Crohn's diseasethan ulcerative colitis. We hypothesize that thedecreased percentage expression and increased MFI ofCD11a, CD18, and ICAM-3 may suggest that cellsup-regulate these ligands following activation and areegressing into tissue.