ABSTRACT
Tissue damage caused by cigarette smoking, at a molecular level, results from leukocyte-mediated damage of the endothelium and subendothelium. Circulating leukocytes are recruited from the circulation and adhere to the vascular endothelium. Following cellular adhesion, the leukocytes migrate to the subendothelium and cause infl ammatory injury to the underlying tissues. Adhesion molecules mediate the interactions between infl ammatory cells, specifi cally circulating leukocytes, and the endothelium. Changes in the expression of these molecules alter the balance between homeostasis and disease. Adhesion molecules are present in two forms: those bound to the epithelial cells and those found in a soluble form, circulating within the blood or other body fl uids. Soluble adhesion molecules have been studied as biomarkers for disease activity and for possible usefulness as prognostic indicators.
