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.