| First Author | Hatfield CA | Year | 1997 |
| Journal | Am J Physiol | Volume | 273 |
| Issue | 3 Pt 1 | Pages | L513-23 |
| PubMed ID | 9316484 | Mgi Jnum | J:43213 |
| Mgi Id | MGI:1097348 | Doi | 10.1152/ajplung.1997.273.3.L513 |
| Citation | Hatfield CA, et al. (1997) Intercellular adhesion molecule-1-deficient mice have antibody responses but impaired leukocyte recruitment. Am J Physiol 273(3 Pt 1):L513-23 |
| abstractText | 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. |
