ABSTRACT
Asthma is a common chronic disease causing narrowing of the bronchial tree; it is characterized by acute episodes of bronchial constriction and increased mucus production, linked to an underlying airways hypersensitivity. Basic research has begun to focus on the mechanisms of infiltration and activation within the lung of eosinophils and mononuclear leukocytes, which contribute to and characterize the underlying inflammatory state. Because adhesion molecules play key roles in this process, much attention has focused on their role in leukocyte recruitment and activation in vivo. Recent evidence indicates a role for integrins in the inhibition of apoptosis of anchorage-dependent cells, such as epithelial and endothelial cells. Integrins may work at multiple levels, including leukocyte recruitment into the tissue itself; migration of cells within the inflamed tissue; priming and activation via ligation to matrix, particularly inflammatory matrix such as alternately spliced fibronectin; and more speculatively through inhibition of apoptosis.
