Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/54294
Title: In vivo inhibition of inducible nitric oxide synthase decreases lung injury induced by Toxocara canis in experimentally infected rats
Authors: Espinoza, Elsa Y.
Pérez-Arellano, José L. 
Carranza, Cristina
Collía, Francisco
Muro, Antonio
Keywords: Hypersensitivity Pneumonitis
Brugia-Malayi
Activated Macrophages
Alveolar Macrophages
Schistosoma-Mansoni, et al
Issue Date: 2002
Publisher: 0141-9838
Journal: Parasite Immunology 
Abstract: The direct effect of nitric oxide (NO) on the viability of Toxocara canis larvae was studied. We observed that the nitric oxide donors, SIN-1 and SNOG, exert no cytotoxic effect on the in vitro viability of T. canis larvae. In addition, we developed a model in rats to elucidate the role of NO during T. canis infection. We evaluated different indicators in four experimental groups: morphological parameters, the total number cells and cell types recovered, nitrite and protein concentration, lactate dehydrogenase and alkaline phosphatase enzymatic activity in the bronchoalveolar lavage fluid, lung index and detection of anti- T. canis specific antibodies. We observed significant differences between non-infected and infected groups. The infected animals treated with the inducible nitric oxide synthase (iNOS) inhibitor aminoguanidine were less damaged than infected, non-treated animals. Our results suggest that the in vivo inhibition of the synthesis of NO triggered by iNOS diminishes the deleterious effects of the parasite upon the host, especially the vascular alterations in the lungs. We could show that in vivo production of NO induced by infection with T. canis results in direct host damage. Thus, this induction may constitute an evasion/adaptation mechanism of the parasite.
URI: http://hdl.handle.net/10553/54294
ISSN: 0141-9838
DOI: 10.1046/j.1365-3024.2002.00598.x
Source: Parasite Immunology[ISSN 0141-9838],v. 24, p. 511-520
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