Integrins in Pulmonary Inflammatory Diseases

• Published in: Current pharmaceutical design Vol. 11; no. 7; pp. 893 - 901
• Main Authors: Bazan-Socha, S, Bukiej, A, Marcinkiewicz, C, Musial, J
• Format: Journal Article
• Language: English
• Published: United Arab Emirates Bentham Science Publishers Ltd 01.01.2005
• Subjects: Animals; Asthma - physiopathology; Disintegrins - therapeutic use; Emphysema - physiopathology; Humans; Integrins - antagonists & inhibitors; Integrins - metabolism; Integrins - physiology; Leukocytes - metabolism; Metalloproteases - therapeutic use; Pneumonia - drug therapy; Pneumonia - physiopathology; Pulmonary Fibrosis - physiopathology; Sarcoidosis - physiopathology
• ISSN: 1381-6128; 1873-4286
• DOI: 10.2174/1381612053381710

Integrins are a family of heterodimeric transmembrane glycoproteins that mediate cell-cell and cell-matrix interactions. They participate in inflammatory reactions mainly by regulation of leukocyte migration, activation and survival. Elevated expression of the cell adhesion molecules, such as VCAM, ICAM and MAdCAM on the lumenal surface of vascular endothelial cells is a critical early event in organ inflammatory processes - including the lung. Adhesive interactions with their counter-receptors on leukocytes, selectins and integrins, result in migration of the leukocytes to the inflammed tissues. Integrins also participate in physiological and pathological reorganization of the lung structure during e.g. pneumonia healing, airway remodeling, angiogenesis, emphysema and pulmonary fibrosis. Agents that could inhibit the function of one or more of these integrins could provide a novel therapeutic strategy targeted to inhibit inflammatory and immune phenomena in the lung.