Upregulation of adhesion molecules in the bronchial mucosa of subjects with chronic obstructive bronchitis.

Abstract

To determine whether adhesion molecules and cytokines are upregulated in the bronchial mucosa of chronic bronchitics, we obtained bronchial biopsies in 16 chronic bronchitics, in eight asymptomatic smokers, and in seven normal nonsmoking subjects. Bronchial biopsies were examined by immunohistochemistry to identify the expression of E-selectin and intercellular adhesion molecular-1 (ICAM-1) on vessels and on bronchial epithelium, and the expression of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), neutrophil elastase, and eosinophil cationic protein (EG-2) on cells in the submucosa. Chronic bronchitics had an increased number of E-selectin-positive vessels when compared with both asymptomatic smokers (p < 0.05) and normal subjects (p < 0.01). The numbers of ICAM-1-positive vessels, neutrophils, and IL-1 beta, TNF-alpha-, and EG-2-positive cells were not significantly different in the three groups of subjects examined. When the bronchitic group was divided according to the presence or absence of airway obstruction, the increased number of E-selectin-positive vessels persisted only in bronchitics with airway obstruction, who also had an increased expression of ICAM-1 on basal epithelial cells. We concluded that in the bronchial mucosa of chronic bronchitics with airway obstruction, there is an increased expression of E-selectin on vessels and of ICAM-1 on basal epithelial cells, suggesting the involvement of these adhesion molecules in the pathogenesis of the disease.

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

“…bronchiolitis [11]. This report established clear differences between smokers and nonsmokers and less marked differences between smokers with or without airways obstruction.…”

“…Recent reports of studies on bronchial biopsies from normal nonsmokers, asymptomatic smokers and smokers with chronic bronchitis and airway obstruction suggest an increased expression of E-selectin in vessels and ICAM-1 on epithelial cells of patients with airways obstruction [11]. However, as this technique only provides tissue from the mucosa of airways that are central to the major site of airways obstruction, we decided to re-examine the problem using resected lung tissue, where all the airways are present.…”

Chronic obstructive pulmonary disease: molecular and cellularmechanisms

“…These serine proteases are also potent mucus stimulants. Neutrophil recruitment to the airways and parenchyma involves adhesion to endothelial cells and E-selectin is upregulated on endothelial cells in the airways of COPD patients [50]. Adherent neutrophils then migrate into the respiratory tract under the direction of neutrophil chemotactic factors, which include interleukin (IL)-8 and leukotriene B 4 (LTB 4 ).…”

Pathogenesis of Chronic Obstructive Pulmonary Disease

“…Once sequestered, neutrophils adhere to endothelial cells, and the adhesion molecule E-selectin has been shown to be upregulated in the airway epithelial cells of patients with COPD (26). Neutrophils can then migrate to the respiratory tract under the control of chemotactic factors, such as leukotriene B 4 , interleukin 8 (IL-8), and related CXC chemokines, including growthrelated oncogene-␣ and epithelial cellϪderived neutrophil attractant 78.…”