CD11b blockade prevents lung injury despite neutrophil priming after gut ischemia/reperfusion

K. Koike, E. E. Moore, F. A. Moore, R. J. Franciose, B. Fontes, F. J. Kim, W. J. Mileski, S. R. Shackford, R. V. Maier, H. O. Rennekampff

Research output: Contribution to journalArticlepeer-review

57 Scopus citations


Gut ischemia/reperfusion (I/R) provokes lung injury via a mechanism that involves neutrophils [polymorphonuclear neutrophils (PMNs)]. CD11b/CD18 (αmB2) is the integrin receptor on PMNs critical for adhesion-dependent oxidative burst. The purpose of this study was to investigate the mechanistic role of CD11b in the process of gut I/R-induced lung injury. Sprague-Dawley rats underwent 45 minutes of superior mesenteric artery (SMA) occlusion with and without CD11b monoclonal antibody treatment (IB6) (1 mg/kg, IV), before SMA clamping. At 2-hour reperfusion, PMN presence in tissue was quantitated by myeloperoxidase activity and circulating PMN priming determined by the difference in superoxide production with and without N-formyl-methionyl- leucyl-phenylalanine, whereas lung leak was assessed by 125I-albumin lung/blood ratio. In sum, CD11b blockade prevented gut I/R-induced lung leak, but did not attenuate gut I/R-induced PMN priming or tissue PMN accumulation. In conclusion, gut I/R promotes PMN priming and PMN adhesion in both local and distant beds via receptors other than CD11b, but this B2 integrin receptor is critical for PMN-mediated endothelial injury.

Original languageEnglish (US)
Pages (from-to)23-26
Number of pages4
JournalJournal of Trauma - Injury, Infection and Critical Care
Issue number1
StatePublished - 1995
Externally publishedYes

ASJC Scopus subject areas

  • Surgery
  • Critical Care and Intensive Care Medicine


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