EXPRESSION OF EPIDERMAL GROWTH-FACTOR AND EPIDERMAL GROWTH-FACTOR RECEPTOR IMMUNOREACTIVITY IN THE ASTHMATIC HUMAN AIRWAY

Chronic airway inflammation, one of the pathophysiologic features of b ronchial asthma, is suspected to be responsible for irreversible patho logical changes of airways, called airway remodeling. To examine the m echanisms of airway remodeling in asthma, we investigated the expressi on of epidermal growth factor (EGF) and its receptor immunohistochemic ally in asthmatic human airways. Airway specimens from seven patients with asthma were obtained from autopsied and surgically resected lungs . Control specimens were obtained from lungs of eight subjects without asthma and other pulmonary complications at autopsy. We stained those specimens by the avidin-biotin-peroxidase complex (ABC) method with a nti-human polyclonal EGF antibody and monoclonal EGF receptor antibodi es. Three different portions of airways-large bronchi (about 1 cm in d iameter), small bronchi (about 3 mm in diameter), and peripheral airwa ys (less than 2 mm in diameter)-were examined. The thickness of the br onchial smooth muscle and basement membrane was significantly greater in the asthmatic airways than in controls. Clear immunoreactivities of EGF were widely observed on bronchial epithelium, glands, and smooth muscle in asthmatic airways. In the controls, the bronchial epithelium and the bronchial glands partially expressed faint EGF immunoreactivi ty. For the EGF receptor, clear, immunoreactivities were also observed on bronchial epithelium, glands, smooth muscle, and basement membrane in asthmatic airways. In control airways, only part of the bronchial epithelium and smooth muscle weakly expressed EGF receptor immunoreact ivity. These results suggest a possible contribution of EGF to the pat hophysiology of bronchial asthma, including airway remodeling.