AJP - Lung Cellular and Molecular Physiology, Vol 273, Issue 3 513-L523, Copyright © 1997 by American Physiological Society

ARTICLES

Intercellular adhesion molecule-1-deficient mice have antibody responses but impaired leukocyte recruitment

C. A. Hatfield, J. R. Brashler, G. E. Winterrowd, F. P. Bell, R. L. Griffin, S. F. Fidler, K. P. Kolbasa, J. L. Mobley, K. L. Shull, I. M. Richards and J. E. Chin
Pharmacia and Upjohn, Kalamazoo, Michigan 49001, USA.

The role of intercellular adhesion molecule-1 (ICAM-1) in murine lung inflammation was examined in vivo. Ovalbumin (Ova)-sensitized and -challenged ICAM-1-deficient (KO) mice had decreased accumulation of leukocytes 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 immunoglobulin (Ig) G1 and higher concentrations of IgE in KO versus WT mice. Ova-dependent induction of cytokines in vitro, as measured by enzyme-linked immunosorbent assay, was impaired in splenocytes from KO mice 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 tissue nuclear factor-kappa B was diminished in KO mice after Ova provocation. This suggests that ICAM-1 was important for activation of the inflammatory cascade leading to the recruitment of leukocytes but was not critical for the generation of antibody responses in vivo.

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