Acute Trypanosoma cruzi experimental infection induced renal ischemic/reperfusion lesion in mice

Acute Trypanosoma cruzi experimental infection induced renal ischemic/reperfusion lesion in mice

Author Oliveira, Gabriel Melo de Google Scholar
Silva, Tshaca Mahatma da Google Scholar
Batista, Wanderson Silva Google Scholar
Franco, Marcello Autor UNIFESP Google Scholar
Schor, Nestor Autor UNIFESP Google Scholar
Institution Fiocruz MS
Universidade Federal de São Paulo (UNIFESP)
Abstract Experimental acute infection with Trypanosoma cruzi in mice promotes an intense myocarditis and other systemic changes. However, the network of pathophysiological disorders and renal injury caused by the infection has not been elucidated. Our previous results with a murine model observed a discrete acute myocarditis and high mortality with significant inflammatory kidney injury with T. cruzi infection. the aim of this study was to investigate the mechanisms of kidney injury caused by the parasite in mice during the experimental acute phase. Results employing BALB/c mice infected with T. cruzi of Y strain showed renal injury on the 6th day postinfection (dpi) caused by a transitory decrease of renal blood flow. Acute kidney injury (AKI) was also observed similar to the model of ischemia/reperfusion lesion in these infected mice. the injury was not related to the presence (or multiplication) of parasites. Only rare nests were microscopically detected, and the presence of scattered parasites in renal parenchyma was seen on the 15th dpi. Thus, it was observed that during the acute phase of the disease, AKI in infected mice is linked to early cardiovascular effects, including heart failure, caused by striking inflammatory lesions in the myocardium, which lead to the high mortality rate of animals.
Language English
Date 2009-12-01
Published in Parasitology Research. New York: Springer, v. 106, n. 1, p. 111-120, 2009.
ISSN 0932-0113 (Sherpa/Romeo, impact factor)
Publisher Springer
Extent 111-120
Access rights Closed access
Type Article
Web of Science ID WOS:000272046200015

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