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

Citation
Lb. Guerra et al., Cyclophosphamide-induced immunosuppression protects cardiac noradrenergic nerve terminals from damage by Trypanosoma cruzi infection in adult rats, T RS TROP M, 95(5), 2001, pp. 505-509
Citations number
30
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Envirnomentale Medicine & Public Health","Medical Research General Topics
Journal title
TRANSACTIONS OF THE ROYAL SOCIETY OF TROPICAL MEDICINE AND HYGIENE
ISSN journal
0035-9203 → ACNP
Volume
95
Issue
5
Year of publication
2001
Pages
505 - 509
Database
ISI
SICI code
0035-9203(200109/10)95:5<505:CIPCNN>2.0.ZU;2-6
Abstract
Trypanosoma cruzi-infected juvenile rats develop severe cardiac sympathetic denervation in parallel with acute myocarditis. This aspect has not been s tudied in adult rats, thought to be resistant to this infection. The mechan ism involved in T. cruzi-induced neuronal damage remains to be completely e lucidated. In juvenile rats, the mortality during the acute phase depends o n T. cruzi populations, ranging from 30% to 100%. Therefore, studies of mec hanisms through hazardous procedures such as immunosuppression are restrict ed. The current paper shows that adult rats infected with T. cruzi (Y strai n) develop severe acute myocarditis and cardiac sympathetic denervation, de spite null mortality and virtual absence of patent parasitaemia followed by negative haemoculture. Recovery from the myocarditis and denervation occur red but PCR studies showed persistence of parasite DNA at least until day 1 11 post inoculation. Immunosuppression by cyclophosphamide treatment increa sed the parasitaemia, prevented the acute myocarditis and the sympathetic d enervation without significant alteration of the myocardial parasitism. The se results argue against a direct role for parasite-derived products and im plicate the inflammatory cells in the denervation process. As previous stud ies in juvenile animals have discarded an essential role for radiosensitive cells, the macrophages remain as the possible effectors for the T. cruzi-i nduced neuronal damage.