Abstract: Poster Presentations |

Expression of Apoptosis-Regulatory Genes in Epithelial Cells in Patients With Idiopathic Pulmonary Fibrosis FREE TO VIEW

Maria Plataki, MD; Anastassios Koutsopoulos, MD; John Drossitis, MD; George Delides, Prof; Nikolaos M. Siafakas, Prof; Demosthenes Bouros, Prof
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Dept of Pneumonology, University General Hospital of Crete, Voutes Heraklion, Greece


Chest. 2003;124(4_MeetingAbstracts):192S-b-193S. doi:10.1378/chest.124.4_MeetingAbstracts.192S-b
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PURPOSE:  Idiopathic pulmonary fibrosis (IPF) begins in the alveolus with epithelial cell injury and alveolar inflammation. Increased apoptosis of the pulmonary epithelial cells could be involved in the pathogenesis of the disease. We studied the expression of apoptotic markers in patients with IPF.

METHODS:  We examined by immunohistochemistry (IHC) the expression of p53, bax (proapoptotic proteins), bcl-2 (antiapoptotic protein) and caspase 3 (effector of apoptosis) in association with DNA strand breaks detected by terminal deoxynucleotidyl transferase-mediated deoxyuridinetriphosphate nick endlabelling (TUNEL) in bronchial and alveolar epithelial cells taken by biopsy in 12 patients with IPF and 10 controls.

RESULTS:  Results are shown in the next tableTUNELp53bcl-2baxCaspase-3IPF91.583.45883.4100Controls201010020100as percentage (%) of subjects showing positive signals in alveolar or bronchial epithelial cells.IHC for bcl-2 and bax in IPF patients was positive in a very small percentage of epithelial cells (<10%). Whereas only in 30% of controls, caspase 3 was positive in >10% of hyperplastic epithelial cells, it was positive in >10% of epithelial cells in 66.7% of IPF patients.CONCLUSIONS: These results show that apoptotic hyperplastic epithelial cells are present in patients with IPF and that the expression of p53, bax and caspase 3 appears to be upregulated and that of bcl-2 downregulated in these cells.

CLINICAL IMPLICATIONS:  Despite current treatment approaches, IPF remains a progressive and fatal disease. Understanding its pathogenesis will improve therapeutic strategies.

DISCLOSURE:  M. Plataki, None.

Wednesday, October 29, 2003

12:30 PM - 2:00 PM




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