Production of superoxide by macrophages from Plasmodium chabaudi infected mice

In vitro superoxide production by spleen and peritoneal macrophages was assessed as a function of Plasmodium chabaudi infection in the mouse. Within the first 5 days post-infection, as parasitaemia rose, there was an increase in phorbolmyristate acetate-triggered superoxide generation by the spleen macrophages. The ability of the macrophages to produce O2- began to decline as the parasite burden increased and at peak it fell to control (pre-infection) levels. This refractory period may have resulted from a desensitization of the macrophage response to PMA triggering. After day 10, as parasitaemia declined, the O2- generation increased once more until day 17. Peritoneal macrophages showed increased ability to produce O2- on PMA triggering during the course of infection and this persisted longer than with spleen macrophages. These data are consistent with an involvement of O2-, or other products derived therefrom, in the killing of plasmodia, as well as in the pathology of malaria.