Trypanosoma brucei is protected from the cytostatic effects of nitric oxide under in vivo conditions

N. A. Mabbott; I. A. Sutherland; J. M. Sternberg

doi:10.1007/BF00932954

Trypanosoma brucei is protected from the cytostatic effects of nitric oxide under in vivo conditions

N. A. Mabbott, I. A. Sutherland, J. M. Sternberg^*

^*Corresponding author for this work

Aberdeen Centre For Environmental Sustainability

Research output: Contribution to journal › Article › peer-review

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Abstract

In mice infected with Trypanosoma brucei, splenic and peritoneal macrophages release substantial amounts of nitric oxide (NO). The production of NO by activated macrophages has been reported to be a nonspecific immune-effector mechansism against several parasites, and in this work we investigate the role of NO in killing T. brucei. Addition of bloodstream trypanosomes to peritoneal macrophages activated in vitro resulted in an NO-dependent inhibition of parasite growth. This effect was totally abrogated when dilutions of whole blood were included in the cultures, suggesting that bloodstream parasites such as T. brucei are not susceptible to NO-mediated killing in vivo.

Original language	English
Pages (from-to)	687-690
Number of pages	4
Journal	Parasitology Research
Volume	80
Issue number	8
DOIs	https://doi.org/10.1007/BF00932954
Publication status	Published - 1 Aug 1994

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10.1007/BF00932954

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abstract = "In mice infected with Trypanosoma brucei, splenic and peritoneal macrophages release substantial amounts of nitric oxide (NO). The production of NO by activated macrophages has been reported to be a nonspecific immune-effector mechansism against several parasites, and in this work we investigate the role of NO in killing T. brucei. Addition of bloodstream trypanosomes to peritoneal macrophages activated in vitro resulted in an NO-dependent inhibition of parasite growth. This effect was totally abrogated when dilutions of whole blood were included in the cultures, suggesting that bloodstream parasites such as T. brucei are not susceptible to NO-mediated killing in vivo.",

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AU - Sutherland, I. A.

AU - Sternberg, J. M.

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AB - In mice infected with Trypanosoma brucei, splenic and peritoneal macrophages release substantial amounts of nitric oxide (NO). The production of NO by activated macrophages has been reported to be a nonspecific immune-effector mechansism against several parasites, and in this work we investigate the role of NO in killing T. brucei. Addition of bloodstream trypanosomes to peritoneal macrophages activated in vitro resulted in an NO-dependent inhibition of parasite growth. This effect was totally abrogated when dilutions of whole blood were included in the cultures, suggesting that bloodstream parasites such as T. brucei are not susceptible to NO-mediated killing in vivo.

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Trypanosoma brucei is protected from the cytostatic effects of nitric oxide under in vivo conditions

Abstract

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