Adhesion molecule expression in the lung: a comparison between normal and diffuse interstitial lung disease

Cellular adhesion molecules are crucial determinants of the migration of immune effector cells to the tissues. In chronic inflammatory diseases, upregulation of the expression of these molecules may contribute to the persistent inflammatory process. The aim of this study was to determine whether there is evidence of adhesion molecule expression in chronically inflamed lung. Soluble adhesion molecules in bronchoalveolar lavage fluid (BALF) were measured by enzyme-linked immunoassay in 54 patients with chronic interstitial lung diseases and 16 normal controls. Adhesion molecule expression in fibrosing alveolitis (FA) lung and in control lung was assessed using immunohistology and reverse transcription-polymerase chain reaction (RT-PCR) amplification. Soluble intercellular adhesion molecule-1 (ICAM-1) was detected in all but two subjects. There was no difference in ICAM-1 concentration between disease groups and normal subjects. In contrast, soluble E-selectin was detected in 17 of the 70 subjects and was significantly associated with the presence of lung disease (p=0.0173). Furthermore, the presence of soluble E-selectin was associated with a raised lymphocyte percentage in BALF (p=0.0069). Soluble VCAM was only detected in five of the 70 subjects (two normals, three patients). There was no difference in adhesion molecule expression in lung parenchyma between FA and controls assessed by immunohistology and RT-PCR. The most striking finding of our study was the universal expression of intercellular adhesion molecule-1 in both normal and diseased lung, emphasizing the important role of the lung in immune function. Upregulation of E-selectin may contribute to inflammatory cell accumulation in chronic interstitial lung diseases.

This article has been cited by other articles:

				S. Toppila, T. Paavonen, A. Laitinen, L. A. Laitinen, and R. Renkonen Endothelial Sulfated Sialyl Lewis x Glycans, Putative L-Selectin Ligands, Are Preferentially Expressed in Bronchial Asthma but Not in Other Chronic Inflammatory Lung Diseases Am. J. Respir. Cell Mol. Biol., October 1, 2000; 23(4): 492 - 498. [Abstract] [Full Text]

				N. SATO, Y. SUZUKI, K. NISHIO, K. SUZUKI, K. NAOKI, K. TAKESHITA, H. KUDO, N. MIYAO, H. TSUMURA, H. SERIZAWA, et al. Roles of ICAM-1 for Abnormal Leukocyte Recruitment in the Microcirculation of Bleomycin-induced Fibrotic Lung Injury Am. J. Respir. Crit. Care Med., May 1, 2000; 161(5): 1681 - 1688. [Abstract] [Full Text]