Am. J. Respir. Cell Mol. Biol., Volume 18, Number 2, February, 1998 158-167

Involvement of Intercellular Adhesion Molecule-1 in the Antigen-induced Infiltration of Eosinophils and Lymphocytes into the Airways in a Murine Model of Pulmonary Inflammation

Jia En Chin, Greg E. Winterrowd, Cheryl A. Hatfield, John R. Brashler, Robert L. Griffin, Steven L. Vonderfecht, Karen P. Kolbasa, Stephen F. Fidler, Kathy L. Shull, Raymond F. Krzesicki, Kathleen A. Ready, Colin J. Dunn, Laurel M. Sly, Nigel D. Staite, and Ivan M. Richards

Cell Biology and Inflammation Research, and Drug Development Toxicology, Pharmacia and Upjohn Inc., Kalamazoo, Michigan

We investigated the effects of in vivo intraperitoneal treatment with the rat monoclonal antibody (mAb), YN1.7.4 (YN1) against intercellular adhesion molecule-1 (ICAM-1) on the ovalbumin (OA)-inhalation-induced infiltration of leukocytes into the airways of OA-sensitized mice. YN1 (100 to 400 µg) given over a period of 72 h dose-dependently reduced the influx of lymphocytes and eosinophils into the bronchial lumen by > 60% and  70%, respectively, when compared with saline or purified rat IgG-treated controls. Alveolar macrophages (AM) in the bronchoalveolar lavage fluid (BALF) were also decreased by > 50%. Lung tissue inflammation as determined by histopathologic examination was reduced. The number of neutrophils in the blood of OA-sensitized mice 3 days after challenge was significantly increased by treatment with YN1. However, at 24 h and 72 h after OA-challenge, the numbers of eosinophils and mononuclear cells in the bone marrow were reduced by YN1 treatment. Additionally, at 72 h after OA-challenge, the numbers of bone-marrow neutrophils were depressed. BALF levels of interleukin-5 (IL-5) and of IgA were lower for YN1-treated mice than for controls. With increasing doses of YN1, the levels of anti-ICAM-1 mAb in the plasma were proportionally increased. To correlate these results with YN1 treatment, blood and BALF T cells and BALF eosinophils were examined with flow cytometry. Blood T cells from YN1-treated mice were unable to bind phycoerythrin (PE)-labeled anti-ICAM-1 mAb ex vivo. These results implied that ICAM-1 on these cells was bound (occupied) by YN1 administered in vivo. Dose-related decreases were observed in the percentage and mean channel fluorescence (MCF) values of ICAM-1⁺ BALF T cells and eosinophils. The percentages of CD11a⁺ or CD49d⁺ eosinophils were also suppressed. Our data suggest that ICAM-1 is an important molecule involved in the recruitment of leukocytes into the airways of sensitized mice after pulmonary challenge.

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