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Infection and Immunity, April 2001, p. 2252-2259, Vol. 69, No. 4
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.4.2252-2259.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Stage-Dependent Role of Nitric Oxide in Control of Trypanosoma cruzi Infection

Michael Saeftel, Bernhard Fleischer, and Achim Hoerauf*

Department of Immunology, Bernhard Nocht Institute for Tropical Medicine, 20359 Hamburg, Germany

Received 11 May 2000/Returned for modification 14 June 2000/Accepted 3 January 2001

Trypanosoma cruzi, the causative agent of Chagas' disease, is known to be susceptible to nitric oxide (NO)-dependent killing by gamma interferon-activated macrophages. Mice deficient for inducible nitric oxide synthase (iNOS) are highly susceptible to T. cruzi, and inhibition of iNOS from the beginning of infection was reported to lead to an increase in trypomastigotes in the blood and to high mortality. In the present study, we investigated whether NO production is essential for the control of T. cruzi in all phases of the infection. BALB/c mice were treated at different time intervals after T. cruzi infection with an iNOS inhibitor, aminoguanidine or L-N6-(1-iminoethyl)-lysine (L-NIL). Treatment initiated with the beginning of the infection resulted in 100% mortality by day 16 postinfection (p.i.). If treatment was started later during the acute phase at the peak of parasitemia (day 20 p.i.), all the mice survived. Parasitemia was cleared and tissue amastigotes became undetectable in these mice even in the presence of the iNOS inhibitor L-NIL. Inhibition of iNOS in the chronic phase of the infection, i.e., from day 60 to day 120 p.i., with L-NIL did not result in a reappearance of parasitemia. These data suggest that while NO is essential for T. cruzi control in the early phase of acute infection, it is dispensable in the late acute and chronic phase, revealing a fundamental difference in control mechanisms compared to those in infections by other members of the order Kinetoplastida, e.g., Leishmania major.

* Corresponding author. Mailing address: Bernhard Nocht Institute for Tropical Medicine, 20359 Hamburg, Germany. Phone: (49) 40-42818-301. Fax: (49) 40-42818-400. E-mail: hoerauf{at}bni.uni-hamburg.de.

Infection and Immunity, April 2001, p. 2252-2259, Vol. 69, No. 4
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.4.2252-2259.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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