Apoptosis underlies immunopathogenic mechanisms in acute silicosis.
Am J Respir Cell Mol Biol
; 27(1): 78-84, 2002 Jul.
Article
en En
| MEDLINE
| ID: mdl-12091249
ABSTRACT
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.
Buscar en Google
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Silicosis
/
Apoptosis
/
Dióxido de Silicio
/
Ganglios Linfáticos
Tipo de estudio:
Etiology_studies
/
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Am J Respir Cell Mol Biol
Asunto de la revista:
BIOLOGIA MOLECULAR
Año:
2002
Tipo del documento:
Article
País de afiliación:
Brasil