Previous work has implicated both neutrophil-endothelial cell (PMN-EC) adhesion and PMN priming (enhanced superoxide production following activation) in the development of postinjury adult respiratory distress syndrome (ARDS) and multiple organ failure (MOF). CD11B, a member of the integrin family of PMN surface receptors, has been alleged to have a prominent role in these inflammatory PMN-EC processes. The purpose of the present study was to test the hypothesis that CD11B-mediated PMN-EC adhesion is necessary for endotoxin (LPS)-induced PMN priming. Human neutrophils, isolated by Percoll gradient centrifugation, were exposed to LPS (100 ng/mL). At fixed times over 120 minutes (a) superoxide following fMLP activation (i.e., priming), (b) PMN-EC adhesion, and (c) expression of CD11Bwere assayed. Superoxide production was measured by cytochromecreduction, PMN-EC adhesion with indium-labelled PMN adherence to human umbilical vein endothelial cell (HUVEC) monolayer cultures, and CD11Bexpression with fluorescent labelled anti-CD11B(60.1) antibodies. The PMN-EC adhesion was biphasic, with an early maximum at 15 minutes followed by a nadir at 60 minutes and secondary rise through 120 minutes of LPS exposure. CD11Bexpression changed dramatically in temporal association with early PMN-EC adhesion, but the secondary increase in adhesion was associated with only a mild rise in CD11Bexpression. PMN priming increased after a latency of 15 minutes to a maximum of 800 nmol/106cells/min after 60 minutes of LPS exposure. The role of CD11Bin PMN-EC adhesion and PMN priming was further investigated with CD11Bblockade using specific monoclonal anti-CD11Bantibodies at times of maximum priming and adhesion (i.e., 15 and 90 minutes of LPS exposure). CD11Bblockade dramatically reduced adhesion at both 15 and 90 minutes, but had no effect on the priming of PMNs exposed to LPS. In summary, the kinetics of LPS-induced CD11Bexpression correlate temporally with PMN-EC adhesion, but not with the induction of PMN priming. Thus, although CD11Bmay have an important role in LPS-induced PMN-EC adhesion, CD11B-mediated adhesion is not required for PMN priming.