THE ROLES OF CD11 CD18 AND ICAM-1 IN ACUTE PSEUDOMONAS AERUGINOSA-INDUCED PNEUMONIA IN MICE/

Neutrophil accumulation in response to Pseudomonas aeruginosa in the l ungs is mediated through CD11/CD18. This study determined the roles of CD11a, CD11b, and intercellular adhesion molecule (ICAM)-1 in P.aerug inosa-induced pneumonia and compared the function of ICAM-1 using Abs or ICAM-1 mutant mice. Anaesthetized BALB/c mice pretreated with eithe r Abs against CD11a, CD11b, ICAM-1, or rat IgG received intratracheal instillation of P.aeruginosa for 4 h. In other studies, ICAM-1 mutant and wild-type mice received either anti-ICAM-1 Ab or rat IgG followed by instillation of P.aeruginosa, The data show that Abs against CD11a, CD11b, and ICAM-1 in BALB/c mice inhibited neutrophil emigration by 7 9, 81, and 56%, respectively. ICAM-1 mutant mice showed no inhibition of neutrophil emigration compared with wild-type mice, Pretreatment wi th anti ICAM-1 Bb inhibited neutrophil emigration in wild-type (129/Sv xC57) mice by 67% but had no effect in ICAM-1 mutant mice, suggesting that the Ab was acting specifically through recognition of its Ag. We conclude that CD11a and CD11b are required for neutrophil emigration, The observed function of ICAM-1 varies depending on the method by whic h it is inhibited, Abs may overestimate function by altering other cel lular functions or mutant mice may develop alternative pathways of emi gration.