Apoptosis, proliferation, and expression of bcl-2, Fas, and Fas ligand in bronchial biopsies from asthmatics

The in situ apoptosis and the expression of molecules involved in this proc ess, such as Bcl-2, Fas, and its ligand, Fas ligand (FasL), were examined i n bronchial biopsies from healthy control subjects and from steroid-untreat ed or -treated asthmatics, using terminal transferase-mediated deoxyuridylt riphosphate nick-end labeling and immunohistochemical techniques, respectiv ely. Bronchial submucosa from steroid-untreated asthmatics showed an increa se in the number of eosinophils and a decrease in that of apoptotic cells c ompared with that of control subjects, but no significant changes in the nu mber of T lymphocytes or in that of cells expressing Bcl-2, Fas, or Fast. T reatment with steroids reduced airway eosinophilia and augmented the propor tion of apoptotic eosinophils. Compared with control subjects or untreated patients, steroid-treated asthmatics exhibited increased expression of Bcl- 2, Fas, Fast, and of proliferating cell nuclear antigen (PCNA) in their bro nchial epithelium, without changes in the number of apoptotic cells. Moreov er, the intensity of the expression of Bcl-2, Fas, and Fast correlates well with that of PCNA. We conclude that steroids may reduce the inflammatory c ell infiltrate in the bronchial submucosa in part by promoting eosinophil a poptosis and by inducing the expression of Fast on bronchial epithelial cel ls. Treatment with steroids may also augment survival and proliferation of epithelial cells, possibly via the expression of Bcl-2 and PCNA.