The expression of adhesion molecules in cigarette smoke-induced airways obstruction

• Published in: The European respiratory journal Vol. 9; no. 10; pp. 1995 - 2001
• Main Authors: Gonzalez, S, Hards, J, van Eeden, S, Hogg, JC
• Format: Journal Article
• Language: English
• Published: Leeds Eur Respiratory Soc 01-10-1996; Maney
• Subjects: Aged; Antibodies, Monoclonal; Antigens, CD - analysis; Antigens, CD - genetics; Biological and medical sciences; CD11 Antigens - analysis; CD11 Antigens - genetics; CD18 Antigens - analysis; CD18 Antigens - genetics; Cell Adhesion Molecules - analysis; Cell Adhesion Molecules - genetics; E-Selectin - analysis; E-Selectin - genetics; Endothelium - metabolism; Endothelium - pathology; Epithelium - metabolism; Epithelium - pathology; Female; Gene Expression Regulation; Humans; Immunohistochemistry; Integrin alpha4beta1; Integrin beta1 - analysis; Integrin beta1 - genetics; Integrins - analysis; Integrins - genetics; Intercellular Adhesion Molecule-1 - analysis; Intercellular Adhesion Molecule-1 - genetics; L-Selectin - analysis; L-Selectin - genetics; Leukocytes - metabolism; Leukocytes - pathology; Lung - metabolism; Lung - pathology; Lung Diseases, Obstructive - genetics; Lung Diseases, Obstructive - metabolism; Lung Diseases, Obstructive - pathology; Male; Medical sciences; Middle Aged; P-Selectin - analysis; P-Selectin - genetics; Pneumonia - genetics; Pneumonia - metabolism; Pneumonia - pathology; Receptors, Lymphocyte Homing - analysis; Receptors, Lymphocyte Homing - genetics; Receptors, Very Late Antigen - analysis; Receptors, Very Late Antigen - genetics; Smoke; Smoking - genetics; Smoking - metabolism; Smoking - pathology; Tobacco, tobacco smoking; Toxicology; Vascular Cell Adhesion Molecule-1 - analysis; Vascular Cell Adhesion Molecule-1 - genetics; Immunohistochemistry; Human; Lung disease; Pathophysiology; Respiratory disease; Tobacco smoking; Exploration; Inflammation; Gene expression; Pathology; Bronchus disease; Complication; Obstructive pulmonary disease
• ISSN: 0903-1936; 1399-3003
• DOI: 10.1183/09031936.96.09101995

Cigarette smoking produces peripheral airway inflammation in all smokers, and chronic airways obstruction in approximately 20% of heavy smokers. The present study was designed to test the hypothesis that airways obstruction is related to changes in the expression of adhesion molecules involved in the recruitment of cells to sites of inflammation in the lung. Freshly resected lungs from heavy smokers with airways obstruction (n = 10) and from heavy smokers with normal lung function (n = 10) were collected in the operating room, inflated with optimal cutting temperature (OCT) medium and frozen over liquid nitrogen. Six micrometres thick cryostat sections cut from random samples of this tissue were stained, using immunohistochemistry, with monoclonal antibodies to the adhesion molecules on leucocytes: L-selectin, very late activation antigen-4 (VLA-4), CD11a/CD18, CD11b/CD18, CD11c/CD18; and on endothelial and epithelial surfaces: E-selectin, P-selectin, vascular cell adhesion molecule (VCAM-1), intercellular adhesion molecule (ICAM)-1 and ICAM-2 using the alkaline phosphatase anti-alkaline phosphatase (APAAP) technique. The slides were coded and the expression of each molecule scored by three observers using a semiquantitative grading system. Two inducible adhesion molecules, E-selectin on endothelium and CD11b on leucocytes, were also evaluated using quantitative morphometric analysis. The results showed a distribution of adhesion molecules that was consistent with the inflammatory response in the airways and parenchyma of all subjects but failed to show any differences between those with or without airways obstruction. We conclude that development of airways obstruction in heavy smokers cannot be explained by differences in the expression of adhesion molecules known to be involved in the control of cell traffic in the lung.