Experimental inhibition of nitric oxide increases Plasmodium relictum (lineage SGS1) parasitaemia.
Exp Parasitol
; 132(4): 417-23, 2012 Dec.
Article
em En
| MEDLINE
| ID: mdl-23022523
ABSTRACT
Malaria is a widespread vector-borne disease infecting a wide range of terrestrial vertebrates including reptiles, birds and mammals. In addition to being one of the most deadly infectious diseases for humans, malaria is a threat to wildlife. The host immune system represents the main defence against malaria parasites. Identifying the immune effectors involved in malaria resistance has therefore become a major focus of research. However, this has mostly involved humans and animal models (rodents) and how the immune system regulates malaria progression in non-model organisms has been largely ignored. The aim of the present study was to investigate the role of nitric oxide (NO) as an immune effector contributing to the control of the acute phase of infection with the avian malaria agent Plasmodium relictum. We used experimental infections of domestic canaries in conjunction with the inhibition of the enzyme inducible nitric oxide synthase (iNOS) to assess the protective function of NO during the infection, and the physiological costs paid by the host in the absence of an effective NO response. Our results show that birds treated with the iNOS inhibitor suffered from a higher parasitaemia, but did not pay a higher cost of infection (anaemia). While these findings confirm that NO contributes to the resistance to avian malaria during the acute phase of the infection, they also suggest that parasitaemia and costs of infection can be decoupled.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Canários
/
Parasitemia
/
Pardais
/
Malária Aviária
/
Óxido Nítrico
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
Exp Parasitol
Ano de publicação:
2012
Tipo de documento:
Article
País de afiliação:
França