Abstract |
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.
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Authors | Zhong Su, Anny Fortin, Philippe Gros, Mary M Stevenson |
Journal | The Journal of infectious diseases
(J Infect Dis)
Vol. 186
Issue 9
Pg. 1321-9
(Nov 01 2002)
ISSN: 0022-1899 [Print] United States |
PMID | 12402202
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
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Topics |
- Acute Disease
- Animals
- Humans
- Macrophages, Peritoneal
(immunology)
- Malaria
(immunology, prevention & control)
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Opsonin Proteins
(immunology)
- Phagocytosis
(physiology)
- Plasmodium chabaudi
(immunology, pathogenicity, physiology)
- Time Factors
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