THE EXPRESSION OF ADHESION MOLECULES IN CIGARETTE SMOKE-INDUCED AIRWAYS OBSTRUCTION

Cigarette smoking produces peripheral airway inflammation in all smoke rs, and chronic airways obstruction in approximately 20% of heavy smok ers, The present study was designed to test the hypothesis that airway s obstruction is related to changes in the expression of adhesion mole cules involved in the recruitment of cells to sites of inflammation in the lung. Freshly resected lungs from heavy smokers with airways obst ruction (n=10) and from heavy smokers with normal lung function (n=10) were collected in the operating room, inflated with optimal cutting t emperature (OCT) medium and frozen over liquid nitrogen, Six micrometr e 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 an tigen-4 (VLA-4), CD11a/CD18, CD11b/CD18, CD11c/CD18; and on endothelia l and epithelial surfaces: E-selectin, P-selectin, vascular cell adhes ion molecule (VCAM-1), intercellular adhesion molecule (ICAM)-1 and IC AM-2 using the alkaline phosphatase anti-alkaline phosphatase (APAAP) technique. The slides were coded and the expression of each molecule s cored by three observers using a semiquantitative grading system, Two inducible adhesion molecules, E-selectin on endothelium and CD11b on l eucocytes, were also evaluated using quantitative morphometric analysi s. The results showed a distribution of adhesion molecules that was co nsistent with the inflammatory response in the airways and parenchyma of all subjects hut failed to show any differences between those with or without airways obstruction. We conclude that development of airway s obstruction in heavy smokers cannot be explained by differences in t he expression of adhesion molecules known to be involved in the contro l of cell traffic in the lung.