PMNS PRIMED FOR SUPEROXIDE RELEASE AND INCREASED CD11B EXPRESSION DO NOT SEQUESTER IN NORMAL LUNG

Our previous work has implicated platelet activating factor (PAF)-indu ced neutrophil (PMN) priming and increased CD11b/CD18 receptor express ion in the pathogenesis of lung injury following gut ischemia/reperfus ion (I/R). In this model CD11b blockade abrogates lung injury but does not alter PMN priming or pulmonary leukosequestration. We, therefore, hypothesized that PAF-stimulated PMN priming and CD11b expression are insufficient to promote lung PMN sequestration. Normal rat PMNs, labe led with Cr-51, were incubated with PAF (10 ng/ml) to induce priming f or superoxide (O-2-) generation and enhance CD11b expression. Gut I/R animals underwent superior mesenteric artery occlusion for 45 min. Cr- 51-labeled PMNs (2 X 10(7)) were injected iv. Study groups, consisting of (a) normal/control, (b) sham/laparotomy, and (c) gut I/R, were giv en either normal or PAF-treated PMNs. PAF-primed PMNs had increased (- )(2) release and CD11b expression, but did not sequester in the lungs of normal rats. However, following gut I/R PAF-treated PMNs sequestere d in the pulmonary bed. These data suggest that PAF priming for O-2- g eneration and increased CD11b expression are insufficient alone to pro mote PMN sequestration in the lung. Rather, additional factors generat ed by gut I/R are necessary for this process. (C) 1995 Academic Press, Inc.