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Immune modulation by fish kinetoplastid parasites: a role for nitric oxide

Published online by Cambridge University Press:  08 October 2002

J. P. J. SAEIJ ,
W. B. VAN MUISWINKEL ,
A. GROENEVELD  and
G. F. WIEGERTJES
J. P. J. SAEIJ
Affiliation:
Cell Biology and Immunology Group, Wageningen Institute of Animal Sciences, Wageningen University, P. O. Box 338, 6700 AH Wageningen, The Netherlands
W. B. VAN MUISWINKEL
Affiliation:
Cell Biology and Immunology Group, Wageningen Institute of Animal Sciences, Wageningen University, P. O. Box 338, 6700 AH Wageningen, The Netherlands
A. GROENEVELD
Affiliation:
Cell Biology and Immunology Group, Wageningen Institute of Animal Sciences, Wageningen University, P. O. Box 338, 6700 AH Wageningen, The Netherlands
G. F. WIEGERTJES
Affiliation:
Cell Biology and Immunology Group, Wageningen Institute of Animal Sciences, Wageningen University, P. O. Box 338, 6700 AH Wageningen, The Netherlands
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Abstract

Trypanoplasma borreli and Trypanosoma carassii are kinetoplastid parasites infecting cyprinid fish. We investigated the role of nitric oxide (NO) in immune modulation during T. borreli and T. carassii infection of carp. Phagocytic cells from different organs produced NO and serum nitrate levels increased, demonstrating that T. borreli activates NO production in vivo. In contrast, T. carassii did not induce NO production in vivo and inhibited LPS-induced NO production in vitro. Production of NO was detrimental to the host as T. borreli-infected carp treated with the inducible NO synthase inhibitor aminoguanidine had a higher survival than infected control carp. This detrimental effect can be explained (in part) by the toxicity of NO to cells in vitro as NO inhibited the proliferative response of blood and spleen leukocytes. Head-kidney phagocytes were resistant to the immunosuppressive effects of NO in vitro. The NO-inducing activity of T. borreli may be an adaptation developed to ensure survival and immune evasion in the fish host. Apparently, T. carassii has adopted another strategy by deactivating specific functions of phagocytes. Both strategies may ensure long-term survival of the parasite.

Keywords

nitric oxidefishparasiteimmunosuppressionTrypanosomaTrypanoplasma
Type
Research Article
Information
Parasitology , Volume 124 , Issue 1 , January 2002 , pp. 77 - 86
Copyright
© 2002 Cambridge University Press

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