Am. J. Respir. Cell Mol. Biol., Vol 12, No. 5, 05 1995, 513-519.
Lymphocyte accumulation during Pseudomonas aeruginosa-induced pneumonia in rodents does not require CD11a and intercellular adhesion molecule-1
JL Wiebke, WM Quinlan, NA Doyle, JE Sligh, CW Smith and CM Doerschuk
Department of Pediatrics, Indiana University, Indianapolis 46202-5225, USA.
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.
