TRYPANOSOMA-BRUCEI IS PROTECTED FROM THE CYTOSTATIC EFFECTS OF NITRIC-OXIDE UNDER IN-VIVO CONDITIONS

In mice infected with Trypanosoma brucei, splenic and peritoneal macro phages release substantial amounts of nitric oxide (NO). The productio n of NO by activated macrophages has been reported to be a nonspecific immune-effector mechansism against several parasites, and in this wor k we investigate the role of NO in killing T. brucei. Addition of bloo dstream trypanosomes to peritoneal macrophages activated in vitro resu lted 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.