LYMPHOCYTE ACCUMULATION DURING PSEUDOMONAS AERUGINOSA-INDUCED PNEUMONIA IN RODENTS DOES NOT REQUIRE CD11A AND INTERCELLULAR-ADHESION MOLECULE-1

Citation
Jl. Wiebke et al., LYMPHOCYTE ACCUMULATION DURING PSEUDOMONAS AERUGINOSA-INDUCED PNEUMONIA IN RODENTS DOES NOT REQUIRE CD11A AND INTERCELLULAR-ADHESION MOLECULE-1, American journal of respiratory cell and molecular biology, 12(5), 1995, pp. 513-519
Citations number
23
Categorie Soggetti
Cell Biology",Biology,"Respiratory System
ISSN journal
10441549
Volume
12
Issue
5
Year of publication
1995
Pages
513 - 519
Database
ISI
SICI code
1044-1549(1995)12:5<513:LADPAP>2.0.ZU;2-I
Abstract
During Pseudomonas aeruginosa-induced pneumonia in rodents, the acute infiltrate of neutrophils is followed by accumulation of lymphocytes i n the perivascular connective tissue. The roles of the adhesion molecu les CD11a/CD18 and intercellular adhesion molecule-1 (ICAM-1) in this accumulation of lymphocytes were investigated. The numbers of lymphocy tes in I 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. aerugino sa-induced pneumonia in ICAM-1 mutant mice was compared with that in w ild-type mice. In rats, both a murine anti-rat CD11a antibody and nons pecific 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 lym phocyte accumulation compared with mice given IgG or no antibody. Furt her, there was no attenuation of the lymphocyte accumulation induced b y II aeruginosa in the ICAM-1 mutant mice compared with wild-type mice , either in the total number of lymphocytes or the number of CD4(+), C D8(+), or B cells. We conclude that neither CD11a/CD18 nor ICAM-1 are required for lymphocyte accumulation during P. aeruginosa-induced pneu monia in rodents. The partial inhibition of the lymphocyte accumulatio n in both the anti-CD11a- and IgG-treated rats may be due to nonspecif ic effects of foreign proteins on cellular functions.