Cyclophosphamide-induced immunosuppression protects cardiac noradrenergic nerve terminals from damage by Trypanosoma cruzi infection in adult rats.

摘要: Trypanosoma cruzi-infected juvenile rats develop severe cardiac sympathetic denervation in parallel with acute myocarditis. This aspect has not been studied adult rats, thought to be resistant this infection. The mechanism involved T. cruzi-induced neuronal damage remains completely elucidated. In the mortality during phase depends on cruzi populations, ranging from 30% 100%. Therefore, studies of mechanisms through hazardous procedures such as immunosuppression are restricted. current paper shows that infected (Y strain) myocarditis and denervation, despite null virtual absence patent parasitaemia followed by negative haemoculture. Recovery occurred but PCR showed persistence parasite DNA at least until day 111 post inoculation. Immunosuppression cyclophosphamide treatment increased parasitaemia, prevented without significant alteration myocardial parasitism. These results argue against a direct role for parasite-derived products implicate inflammatory cells process. As previous animals have discarded an essential radiosensitive cells, macrophages remain possible effectors damage.