The importance of leukotrienes in airway inflammation in a mouse model of asthma.

Author:

Henderson W R1,Lewis D B1,Albert R K1,Zhang Y1,Lamm W J1,Chiang G K1,Jones F1,Eriksen P1,Tien Y T1,Jonas M1,Chi E Y1

Affiliation:

1. Department of Medicine, University of Washington, Seattle 98195, USA.

Abstract

Inhalation of antigen in immunized mice induces an infiltration of eosinophils into the airways and increased bronchial hyperreactivity as are observed in human asthma. We employed a model of late-phase allergic pulmonary inflammation in mice to address the role of leukotrienes (LT) in mediating airway eosinophilia and hyperreactivity to methacholine. Allergen intranasal challenge in OVA-sensitized mice induced LTB4 and LTC4 release into the airspace, widespread mucus occlusion of the airways, leukocytic infiltration of the airway tissue and broncho-alveolar lavage fluid that was predominantly eosinophils, and bronchial hyperreactivity to methacholine. Specific inhibitors of 5-lipoxygenase and 5-lipoxygenase-activating protein (FLAP) blocked airway mucus release and infiltration by eosinophils indicating a key role for leukotrienes in these features of allergic pulmonary inflammation. The role of leukotrienes or eosinophils in mediating airway hyperresponsiveness to aeroallergen could not be established, however, in this murine model.

Publisher

Rockefeller University Press

Subject

Immunology,Immunology and Allergy

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