INTERCELLULAR-ADHESION MOLECULE-1-DEFICIENT MICE HAVE ANTIBODY-RESPONSES BUT IMPAIRED LEUKOCYTE RECRUITMENT

The role of intercellular adhesion molecule-1 (ICAM-1) in murine lung inflammation was examined in vivo. Ovalbumin (Ova)-sensitized and -cha llenged ICAM-1-deficient (KO) mice had decreased accumulation of leuko cytes in the bronchoalveolar lavage fluid compared with wild-type (WT) mice. Lung tissue inflammation was also attenuated. Ova immunization and challenge produced equivalent plasma levels of Ova-specific immuno globulin (Ig) G(1) and higher concentrations of IgE in KO versus WT mi ce. Ova-dependent induction of cytokines in vitro, as measured by enzy me-linked immunosorbent assay, was impaired in splenocytes from KO mic e compared with the comparable release of interleukin (IL)-5 and IL-10 from anti-CD3-stimulated WT and KO splenocytes. Methacholine-induced increases in trapped gas in lungs of Ova-sensitized and -challenged WT mice were greater than those of KO mice. The activation of lung tissu e nuclear factor-kappa B was diminished in KO mice after Ova provocati on. This suggests that ICAM-1 was important for activation of the infl ammatory cascade leading to the recruitment of leukocytes but was not critical for the generation of antibody responses in vivo.