CD11B BLOCKADE PREVENTS LUNG INJURY DESPITE NEUTROPHIL PRIMING ALTER GUT ISCHEMIA-REPERFUSION

Gut ischemia/reperfusion (I/R) provokes lung injury via a mechanism th at involves neutrophils [polymorphonuclear neutrophils (PMNs)]. CD11b/ CD18 (alpha mB(2)) is the integrin receptor on PMNs critical for adhes ion-dependent oxidative burst, The purpose of this study was to invest igate the mechanistic role of CD11b in the process of gut I/R-induced lung injury. Sprague-Dawley rats underwent 45 minutes of superior mese nteric artery (SMA) occlusion with and without CD11b monoclonal antibo dy treatment (IB6) (1 mg/kg, IV), before SMA clamping. At 2-hour reper fusion, PMN presence in tissue was quantitated by myeloperoxidase acti vity and circulating PMN priming determined by the difference in super oxide production with and without N-formyl-methionyl-leucyl-phenylalan ine, whereas lung leak was assessed by I-125-albumin lung/blood ratio. In sum, CD11b blockade prevented gut UR-induced lung leak, but did no t attenuate gut I/R-induced PMN priming or tissue PMN accumulation, In conclusion, gut I/R promotes PMN priming and PMN adhesion in both loc al and distant beds via receptors other than CD11b, but this B-2 integ rin receptor is critical for PMN-mediated endothelial injury.