EFFECTS OF TRAUMA ON LEUKOCYTE INTERCELLULAR-ADHESION MOLECULE-1, CD11B, AND CD18 EXPRESSIONS

Background: During traumatic injury, a multitude of events, including ischemia, may cause leukocyte adhesion and margination, In this study, alterations of surface receptors involved in leukocyte adhesion were studied in traumatized patients. In an attempt to discern the role of hypoxia, additional experiments were conducted in which normal human l eukocytes were subjected to hypoxic stress in vitro. Methods: Venous b lood was obtained from 10 trauma patients within 2 hours of blunt inju ry (mean Injury Severity Score of 17 +/- 8) and from 8 normal voluntee rs (controls), Leukocytes were isolated from patients and controls. To assess the effect of hypoxia, normal leukocytes were placed in hermet ically sealed environments containing 100% nitrogen. All leukocytes we re labeled with phycoerythrin- or fluorescein-bound monoclonal antibod ies to intercellular adhesion molecule-1 (ICAM-1), or to integrins CD1 8 and CD11b Receptor concentration was measured by flow cytometry. Res ults were expressed as percentage of receptor-positive cells (%) acid mean fluorescence channel units, which directly correlate with monoclo nal antibody cell surface density, Significance of differences was tes ted by analysis of variance/Kruskal-Wallis test. Results: Compared wit h the normal controls, circulating leukocytes obtained from traumatize d patients showed decreased expression of ICAM-1, CD11b, and CD18 2 ho urs after injury, In contrast, normal leukocytes exposed to hypoxic st ress in vitro exhibited a marked increase in CD11b and CD18 expression and no change in ICAM-1 expression. Conclusions: Leukocytes obtained from traumatized patients showed a significant decrease in cell surfac e expression of adhesion receptors, This phenomenon is unlikely to be a direct consequence of hypoxia alone, because exposure to isolated hy poxia in vitro actually increased expression of CD11b acid CD18.