Data/hora: 08/06/2024 12:28:46

Provedor de dados: | 55
País: | Brazil
Título: | Immune effector mechanisms of the nitric oxide pathway in malaria: cytotoxicity versus cytoprotection
Autores: | Nahrevanian,Hossein.
Data: | 2006-08-01
Ano: | 2006
Palavras-chave: | INOS; Malaria; Nitric oxide; NO; RNI.
Resumo: | Nitric oxide (NO) is thought to be an important mediator and critical signaling molecule for malaria immunopathology; it is also a target for therapy and for vaccine. Inducible nitric oxide synthase (iNOS) is synthesized by a number of cell types under inflammatory conditions. The most relevant known triggers for its expression are endotoxins and cytokines. To date, there have been conflicting reports concerning the clinical significance of NO in malaria. Some researchers have proposed that NO contributes to the development of severe and complicated malaria, while others have argued that NO has a protective role. Infection with parasites resistant to the microbicidal action of NO may result in high levels of NO being generated, which could then damage the host, instead of controlling parasitemia. Consequently, the host-parasite interaction is a determining factor for whether the parasite is capable of stimulating NO production; the role of NO in resistance to malaria appears to be strain specific. It is known that NO and/or its related molecules are involved in malaria, but their involvement is not independent of other immune events. NO is an important, but possibly not an essential contributor to the control of acute-phase malaria infection. The protective immune responses against malaria parasite are multifactorial; however, they necessarily involve final effector molecules, including NO, iNOS and RNI.
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1413-86702006000400014
Editor: | Brazilian Society of Infectious Diseases
Relação: | 10.1590/S1413-86702006000400014
Formato: | text/html
Fonte: | Brazilian Journal of Infectious Diseases  v.10 n.4 2006
Fonte: | info:eu-repo/semantics/openAccess