Lymphocyte accumulation during Pseudomonas aeruginosa-induced pneumonia in rodents does not require CD11a and intercellular adhesion molecule-1.

During Pseudomonas aeruginosa-induced pneumonia in rodents, the acute infiltrate of neutrophils is followed by accumulation of lymphocytes in the perivascular connective tissue. The roles of the adhesion molecules CD11a/CD18 and intercellular adhesion molecule-1 (ICAM-1) in this accumulation of lymphocytes were investigated. The numbers of lymphocytes in P. aeruginosa-induced pneumonia were compared in animals treated with blocking antibodies to either CD11a, ICAM-1, IgG, or no antibody. In other experiments, the lymphocyte accumulation during P. aeruginosa-induced pneumonia in ICAM-1 mutant mice was compared with that in wild-type mice. In rats, both a murine anti-rat CD11a antibody and nonspecific murine IgG partially inhibited the lymphocyte accumulation by 30 to 40% compared with animals that received no antibodies. In mice, blocking antibodies to either CD11a or ICAM-1 did not decrease the lymphocyte accumulation compared with mice given IgG or no antibody. Further, there was no attenuation of the lymphocyte accumulation induced by P. aeruginosa in the ICAM-1 mutant mice compared with wild-type mice, either in the total number of lymphocytes or the number of CD4+, CD8+, or B cells. We conclude that neither CD11a/CD18 nor ICAM-1 are required for lymphocyte accumulation during P. aeruginosa-induced pneumonia in rodents. The partial inhibition of the lymphocyte accumulation in both the anti-CD11a- and IgG-treated rats may be due to nonspecific effects of foreign proteins on cellular functions