Heat shock proteins 70 and 90 expression in peripheral lung of COPD patients

Heat shock proteins (HSP) 70 and 90 are chaperones that play critical roles in many cellular functions. Peripheral lung (small airways and lung parenchyma) is the main site of airflow obstruction in chronic obstructive pulmonary disease (COPD). In animal models HSP-70 and -90 may have roles in the pathogenesis of pulmonary fibrosis and MUC5AC secretion. The aim of our study was to investigate by immunohistochemistry the localization and expression of HSP-70 and -90 in the peripheral lung of smokers with or without COPD compared with non-smoker subjects. Lung tissue was obtained during lung resection surgery. We examined formalin-fixed paraffin-embedded lung sections by immunohistochemistry for identification of HSP-70 and -90+ cells. The number of HSP +ve cells was determined among the alveolar macrophages and in the bronchiolar epithelium. Samples from 8 non-smokers subjects (age: 69.1±3.2, 1M, FEV1/FVC ratio = 80.1±2.3), 26 smokers with normal lung function (age: 67.9±2.3, 22M, 48±9 pack years, FEV1/FVC ratio=77.5±1.3) and 19 smokers with COPD (age: 71.3±1.4, 17M, 45±8 pack years, post-bronchodilator FEV1/FVC ratio=60.1±2.7) were analyzed. We found a significant difference in HSP-90 +ve alveolar macrophages numbers between non-smokers (35.6±9.4% +ve alveolar macrophages/total number alveolar macrophages) and smokers with normal lung function (69.0±5.7% +ve alveolar macrophages/total number alveolar macrophages; p<0.05) but not between non-smokers and smokers with COPD (57.3±7.7% +ve alveolar macrophages/total number alveolar macrophages) nor between smokers with normal lung function and smokers with COPD. No differences were found in HSP-70 expression in the alveolar macrophages. Also, HSP-70 and -90 expression was similar in the bronchiolar epithelium of the 3 groups of subjects. These data indicates HSP-90 is up-regulated in the alveolar macrophages of smokers with normal lung function.