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
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.