Opsonin-independent phagocytosis: an effector mechanism against acute blood-stage Plasmodium chabaudi AS infection.
Opsonin-independent macrophage phagocytosis was investigated as a possible mechanism of controlling early blood-stage Plasmodium chabaudi AS infection. Early during infection, peritoneal macrophages from resistant C57BL/6 (B6) mice exhibited increased phagocytosis of parasitized red blood cells (pRBCs) and free merozoites, which was absent in mice with deficient interferon (IFN)-gamma production during infection, including susceptible A/J, interleukin (IL)-12 p40, and IFN-gamma gene knockout mice. IFN-gamma treatment of macrophages collected from B6 and A/J mice early during infection enhanced phagocytosis of pRBCs, but IL-10 treatment inhibited this function. In vitro and in vivo studies in which type I and II class A scavenger receptor-deficient mice and inhibitors of scavenger and mannose receptors were used revealed that scavenger receptors other than class A type I and II and mannose receptors may play a role in malaria parasite uptake. These results indicate that opsonin-independent phagocytosis contributes to the IFN-gamma-dependent control of acute blood-stage malaria infection.
Su
Zhong
Z
Centre for the Study of Host Resistance, Research Institute of the McGill University Health Centre, Montreal General Hospital, Montreal, Quebec, Canada. zhong.su@mail.mcgill.ca
Fortin
Anny
A
Gros
Philippe
P
Stevenson
Mary M
MM
D000208:Acute Disease; D000818:Animals; D006801:Humans; D017737:Macrophages, Peritoneal / Q000276:immunology; D008288:Malaria / Q000276:immunology* / Q000517:prevention & control; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009895:Opsonin Proteins / Q000276:immunology; D010587:Phagocytosis / Q000502:physiology*; D016788:Plasmodium chabaudi / Q000276:immunology / Q000472:pathogenicity* / Q000502:physiology*; D013997:Time Factors
D009895:Opsonin Proteins