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Parasite killing in murine malaria does not require nitric oxide production

Published online by Cambridge University Press:  01 February 1999

N. FAVRE ,
B. RYFFEL  and
W. RUDIN
N. FAVRE
Affiliation:
Department of Medical Parasitology, Swiss Tropical Institute, Basel, Switzerland Present address: Kanstonsspital Basel, Exp. Nephrologie, Basel, Switzerland.
B. RYFFEL
Affiliation:
Department of Immunology, Medical School, University of Cape Town, South Africa
W. RUDIN
Affiliation:
Department of Medical Parasitology, Swiss Tropical Institute, Basel, Switzerland
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Abstract

Nitric oxide (NO) production has been suggested to play a role as effector molecule in the control of the malarial infections. However, the roles of this molecule are debated. To assess whether blood-stage parasite killing is NO dependent, we investigated the course of blood-stage Plasmodium chabaudi chabaudi (Pcc) infections in inducible nitric oxide synthase (iNOS)-deficient mice. Parasitaemia, haematological alterations, and survival were not affected by the lack of iNOS. To exclude a role of NO produced by other NOS, controls included NO suppression by oral administration of aminoguanidine (AG), a NOS inhibitor. As in iNOS-deficient mice, no difference in the parasitaemia course, survival and haematological values was observed after AG treatment. Our results indicate that NO production is not required for protection against malaria in our murine experimental model. However, C57BL/6 mice treated with AG lost their resistance to Pcc infections, suggesting that the requirement for NO production for parasite killing in murine blood-stage malaria might be strain dependent.

Keywords

malarianitric oxidePlasmodium chabaudiiNOS-deficient mice
Type
Research Article
Information
Parasitology , Volume 118 , Issue 2 , February 1999 , pp. 139 - 143
Copyright
1999 Cambridge University Press

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