Antibody‐dependent neutrophil‐mediated parasite killing in non‐lethal rodent malaria

SUMMARY The effects of administrating recombinant human granulocyte colony‐stimulating factor (rhG‐CSF) and passively transferring immune serum on infection with an attenuated variant of Plasmodium berghei XAT (Pb XAT), in severe combined immunodeficiency (SCID) mice were examined. In immune competent (C.B‐17) mice, the attenuated parasite infection was inevitably self‐resolving and degenerating forms inside erythrocytes appeared, coinciding with the drop in parasitaemia, whereas SCID mice were unable to control parasite growth and all the mice died. Continuous administration with rhG‐CSF caused neutrophilic granulocytosis in both SCID and C.B‐17 mice. The effect of rhG‐CSF on the infection in C.B‐17 mice was to suppress the course of the parasitaemia at an early phase whereas it had no effect in SCID mice. When immune serum was transferred on the day of infection, the prepatent period was prolonged two days in both SCID and C.B‐17 mice. When administration with rhG‐CSF was combined with transfer of immune serum, SCID mice showed four days delay in patency and degenerating parasites were seen during the course of parasitaemia, although the infection was ultimately fatal. C.B‐17 mice similarly treated showed a seven day delay in the onset of the patent parasitaemia which was of a lesser magnitude and shorter in duration compared with control mice. On the other hand, when C.B‐17 mice were splenectomized three weeks before infection and then treated with rhG‐CSF and immune serum, no degenerating parasites were seen during the infection and all mice died with high parasitaemias. These results show that antibody‐dependent neutrophil‐mediated parasite killing may occur in the spleen of mice infected with P. berghei XAT.