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Título: | Interferon-γ induced nitric oxide mediates in vitro neuronal damage by Trypanosoma cruzi-infected macrophages. |
Autor(es): | Leite, Camila Megale Almeida Galvão, Lúcia Maria da Cunha Afonso, Luís Carlos Crocco Cunha, Fernando de Queiroz Arantes, Rosa Maria Esteves |
Palavras-chave: | Nitric oxide Neuron Macrophage |
Data do documento: | 2007 |
Referência: | LEITE, C. M. A. et al. Interferon-γ induced nitric oxide mediates in vitro neuronal damage by Trypanosoma cruzi-infected macrophages. Neurobiology of Disease, v. 25, p. 170-178, 2007. Disponível em: <http://www.sciencedirect.com/science/article/pii/S0969996106002233>. Acesso em: 08 nov. 2014. |
Resumo: | Neuronal lesions and peripheral denervation in Chagas' disease are related to local inflammation; however, the pathogenic mechanisms of neuronal lesions in the heart and megavisceras are still unclear. We investigated the involvement of nitric oxide (NO) on neuronal lesion in co-cultures of neurons and macrophages. Trypanosoma cruzi-infected and interferon-γ (IFN-γ)-activated co-cultures of neurons and wildtype (WT) macrophages showed significant reduction of both neuronal survival and neurite density. These findings correlated with the levels of NO and the expression of inducible nitric oxide synthase (iNOS). Accordingly, neuronal survival rate in the co-cultures was recovered to control levels by treatment of the cultures with the iNOS inhibitor, aminoguanidine. Moreover, neither neuronal survival nor the neurite density was affected in the co-cultures when the macrophages were harvested from iNOS-deficient mice. These results demonstrate that iNOS-derived NO is the major molecule involved in neuronal damage mechanism in our in vitro model of Chagas' disease neuropathology. |
URI: | http://www.repositorio.ufop.br/handle/123456789/4296 |
DOI: | https://doi.org/10.1016/j.nbd.2006.09.003 |
ISSN: | 0969-9961 |
Licença: | O periódico Neurobiology of Disease concede permissão para depósito deste artigo no Repositório Institucional da UFOP. Número da licença: 3520371457568. |
Aparece nas coleções: | DECBI - Artigos publicados em periódicos |
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