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

Autor: I. M. Richards, S. F. Fidler, F. P. Bell, C. A. Hatfield, R. L. Griffin, Jia En Chin, J. L. Mobley, K. P. Kolbasa, J. R. Brashler, G. E. Winterrowd, Kathy L. Shull
Rok vydání: 1997
Předmět:
Zdroj: The American journal of physiology. 273(3 Pt 1)
ISSN: 0002-9513
Popis: 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.
Databáze: OpenAIRE