Expression of adhesion molecules in peripheral pulmonary vessels from smokers and nonsmokers.

INTRODUCTION AND RATIONALE: An accumulation of intraalveolar cells, especially of macrophages and granulocytes, can be observed in smokers. Since adhesion molecules are involved in the process of cell accumulation, in this study we investigated the hypothesis that the expression of endothelial adhesion molecules on pulmonary vascular endothelial cells is different in smokers and nonsmokers.
METHODS: We investigated lung biopsies from 26 patients who underwent thoracic surgery for localized malignancies (smokers: 15; nonsmokers: 11). Cryostat sections were stained by using immunohistochemistry (APAAP method) with antibodies against E- and P-selectin, the vascular adhesion molecule-1 (VCAM-1), and the intercellular adhesion molecule-1 (ICAM-1). The number of adhesion molecule-positive stained vessels was compared to the total number of vessels identified by the expression of von Willebrand's factor (vWF) and anti-CD31.
RESULTS: The two groups investigated showed no differences in the expression of E-, and P-selectin and of VCAM-1. In contrast, the expression of ICAM-1 was significantly increased in smokers (median 25 vessels/section, CI95%: 19-31) compared to nonsmokers (median 16 vessels/section, CI95%: 9-21) (p = 0.030). In smoking subjects, we were also able to demonstrate a positive correlation between the duration of smoking expressed as pack years and the expression of ICAM-1 on pulmonary vessels (Spearman rank coefficient of correlation 0.857; p = 0.0002).
CONCLUSION: The observed increased expression of ICAM-1 on pulmonary vascular endothelial cells in smokers compared to nonsmokers may be involved in the increased recruitment of inflammatory cells to the alveolar space of smokers.