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

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 mechanism 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.