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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

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

J E Chin, G E Winterrowd, C A Hatfield, J R Brashler, R L Griffin, S L Vonderfecht, K P Kolbasa, S F Fidler, K L Shull, R F Krzesicki, K A Ready, C J Dunn, L M Sly, N D Staite, I M Richards

Am J Respir Cell Mol Biol. 1998 Feb;18(2):158-67.

PMID: 9476902

Abstract:

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 microg) given over a period of 72 h dose-dependently reduced the influx of lymphocytes and eosinophils into the bronchial lumen by > 60% and > or = 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- 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.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP75187632	YN1		75187-63-2	Price

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