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CD11b and Intercellular Adhesion Molecule-1 Are Involved in Pulmonary Neutrophil Recruitment in Lipopolysaccharide-Induced Airway Disease

Division of Critical Care, Department of Pediatrics, University of Iowa, Iowa City, Iowa; Department of Veterans Affairs, Durham; and Division of Pulmonary and Critical Care Medicine, Duke University School of Medicine, Durham, North Carolina

Address correspondence to: Jessica G. Moreland, M.D., Division of Pediatric Critical Care, Department of Pediatrics, University of Iowa, Iowa City, IA 52242. E-mail: jessica-moreland{at}uiowa.edu

To better define the roles of CD11b, CD11a, and one of their endothelial cell receptors, intercellular adhesion molecule-1 (ICAM-1), in the lower respiratory tract inflammatory response to inhaled lipopolysaccharide (LPS), we evaluated the physiologic and biologic response to inhaled LPS in mice receiving anti-CD11b antibody, anti-CD11a antibody, and anti–ICAM-1 antibody. Mice receiving anti-CD11b antibody had a dramatic reduction in pulmonary neutrophil recruitment compared with control mice (18,300 versus 143,000 cells/ml, and neutrophils 16.7% versus 77%), whereas mice receiving anti-CD11a antibody did not demonstrate a reduction in lavage cellularity. Mice receiving anti–ICAM-1 antibody also demonstrated a dose-dependent reduction in inflammatory cell recruitment to the alveolar space. Despite the significant reduction in inflammatory cell infiltrate in mice receiving either CD11b or ICAM-1 antibodies, there was no reduction in the development of airway hyperreactivity. These findings suggest that CD11b and ICAM-1 are important mediators of LPS-induced airway inflammation, but do not appear to be critical to the development of LPS-induced airway hyperreactivity.

Abbreviations: airway hyperresponsiveness, AHR • enzyme-linked immunosorbent assay, ELISA • intercellular adhesion molecule-1, ICAM-1 • interleukin, IL • lipopolysaccharide, LPS • macrophage inflammatory protein, MIP • tumor necrosis factor, TNF

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