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Am. J. Respir. Cell Mol. Biol., Volume 19, Number 5, November, 1998 747-757

Apoptosis, Proliferation, and Expression of Bcl-2, Fas, and Fas Ligand in Bronchial Biopsies from Asthmatics

Anne Druilhe, Benoît Wallaert, Anne Tsicopoulos, José-Roberto Lapa e Silva, Isabelle Tillie-Leblond, André-Bernard Tonnel, and Marina Pretolani

Unité de Pharmacologie Cellulaire, Unité Associée Institut Pasteur/INSERM U485, Paris, France; INSERM U416, Institut Pasteur/Service de PneumoImmunoAllergologie, Hôpital Calmette, Lille, France; and Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro, Brazil

The in situ apoptosis and the expression of molecules involved in this process, such as Bcl-2, Fas, and its ligand, Fas ligand (FasL), were examined in bronchial biopsies from healthy control subjects and from steroid-untreated or -treated asthmatics, using terminal transferase-mediated deoxyuridyltriphosphate nick-end labeling and immunohistochemical techniques, respectively. Bronchial submucosa from steroid- untreated asthmatics showed an increase in the number of eosinophils and a decrease in that of apoptotic cells compared with that of control subjects, but no significant changes in the number of T lymphocytes or in that of cells expressing Bcl-2, Fas, or FasL. Treatment with steroids reduced airway eosinophilia and augmented the proportion of apoptotic eosinophils. Compared with control subjects or untreated patients, steroid-treated asthmatics exhibited increased expression of Bcl-2, Fas, FasL, and of proliferating cell nuclear antigen (PCNA) in their bronchial epithelium, without changes in the number of apoptotic cells. Moreover, the intensity of the expression of Bcl-2, Fas, and FasL correlates well with that of PCNA. We conclude that steroids may reduce the inflammatory cell infiltrate in the bronchial submucosa in part by promoting eosinophil apoptosis and by inducing the expression of FasL on bronchial epithelial cells. Treatment with steroids may also augment survival and proliferation of epithelial cells, possibly via the expression of Bcl-2 and PCNA.




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Copyright © 1998 American Thoracic Society. 		  CCM abstracts