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Am. J. Respir. Cell Mol. Biol., Volume 27, Number 1, July, 2002 78-84

Apoptosis Underlies Immunopathogenic Mechanisms in Acute Silicosis

Valeria M. Borges, Marcela F. Lopes, Haroldo Falcão, José Henrique Leite-Júnior, Patricia R. M. Rocco, Wendy F. Davidson, Rafael Linden, Walter A. Zin, and George A. DosReis

Instituto de Biofísica Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil; and Immunology Department, Holland Laboratory, American Red Cross, Rockville, Maryland

We investigated immunopathogenic roles for apoptosis in acute murine silicosis. Intratracheal silica instillation induced pulmonary inflammation and enlarged thoracic lymph nodes. Lymphocytes from silica-exposed lymph nodes showed reduced mitogenic responses to T cell receptor (TCR) stimulation, and markedly increased activation-induced cell death, compared with control lymphocytes from saline-exposed lymph nodes. CD4+ T cell death was mediated by Fas ligand, because CD4+ T cells from Fas ligand-deficient gld mice did not undergo activation-induced apoptosis. Silica deposition also resulted in increased apoptosis associated with inflammatory infiltrates in lung parenchyma. In vivo treatment with caspase inhibitors reduced neutrophil accumulation, and alleviated inflammation in the lungs of silica-treated mice. These results suggest that silica-induced apoptosis plays an inflammatory role in the lung parenchyma, and creates immunologic abnormalities in regional lymph nodes, with pathogenic implications for the host.

Abbreviations: activation-induced cell death, AICD; antigen-presenting cells, APC; Fas ligand, FasL; flow cytometry, FCM; fetal calf serum, FCS; generalized lymphoproliferative disease, gld; lymph node cells, LNC; 3H-TdR, tritiated thymidine; monoclonal antibody, mAb; myeloperoxidase, MPO; phorbol ester, PMA; T cell receptor, TCR; transmission electron microscopy, TEM.




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