Affiliation:
1. Pneumology Hospital A. Mami, Department of Respiratory Diseases, Ariana, Tunisia
2. Homeostasis and Cell Dysfunction Unit Research 99/UR/08-40, Medicine University of Tunis, 15 Rue Djebel Lakhdar, Tunis 1007, Tunisia
Abstract
Objective:To understand the role of apoptosis through Fas/Fas ligand (FasL) interaction in the pathogenesis of silicosis, we examined the expression of Fas antigen, FasL and apoptosis in bronchoalveolar lavage fluid lymphocytes obtained from patients with silicosis.Materials and methods:Ten patients with silicosis, and 10 healthy controls were studied. Non-adherent cells were separated and analysed by cytometry for the expression of Fas antigen, FasL, and the co-expression of Fas/FasL. By double staining, we studied the FasL expression on CD4, CD8, CD56 and CD45RO-positive cells. DNA fragmentation was investigated by the terminal deoxy(d) UTP nick end labelling (TUNEL) method.Results:We have found Fas and FasL expression in silicosis patients to be significantly higher than those in healthy controls. Interestingly, 6-18% of lymphocytes from silicosis patients co-expressed Fas and FasL. In silicosis patients, FasL was highly expressed on CD4+, CD56+and CD45RO+bronchoalveolar lavage cells. Fas antigen expressing cells showed DNA fragmentation characteristic for apoptosis.Conclusion:FasL was significantly expressed on cytotoxic effector and memory cells. The Fas/FasL system is implicated in the inflammatory process observed in silicosis patients.
Funder
Ministère de l’enseignement Supérieur et de La Recherche et de La Technologie
Cited by
8 articles.
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