Molecular mechanism of T-cell control of Chlamydia in mice: role of nitric oxide in vivo.
Immunology
; 88(1): 1-5, 1996 May.
Article
em En
| MEDLINE
| ID: mdl-8707333
ABSTRACT
T-cell-mediated immunity is crucial for the control of Chlamydia in mice. Recent evidence from studies in an in vitro model of the mucosal epithelium, the polarized epithelial-lymphocyte co-culture (PELC) system, indicated that protective murine T cells mediated intracellular inhibition of the Chlamydia trachomatis agent of mouse pneumonitis (MoPn) at least partly by activating the interferon-gamma (IFN-gamma)-inducible nitric oxide synthase (iNOS) pathway. To investigate whether nitric oxide played a role in controlling chlamydial infection in vivo, the protective capacity of a chlamydial-specific T-cell clone (clone 2.14-0) was analysed in mice in the presence of a specific inhibitor of iNOS. The results revealed that the ability of this clone to clear Chlamydia in vivo is in part mediated by induction of nitric oxide (NO) production. The L-arginine analogue and iNOS inhibitor, NG-monomethyl-L-arginine monoacetate (MLA), increased the chlamydial burden in infected mice and inhibited the ability of clone 2.14-0 to clear genital MoPn infection in vivo. The results are consistent with the working hypothesis that the IFN-gamma-inducible iNOS pathway is involved in the control of Chlamydia by T lymphocytes in mice.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Infecções por Chlamydia
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Chlamydia trachomatis
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Linfócitos T Auxiliares-Indutores
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Óxido Nítrico
Idioma:
En
Ano de publicação:
1996
Tipo de documento:
Article