Opsonin-independent phagocytosis:: An effector mechanism against acute blood-stage Plasmodium chabaudi AS infection
Opsonin-independent phagocytosis:: An effector mechanism against acute blood-stage Plasmodium chabaudi AS infection
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DOI：
10.1086/344576
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发表时间：
2002-11-01
影响因子：
6.4
通讯作者：
Stevenson, MM
中科院分区：
文献类型：
--
作者：
Su, Z;Fortin, A;Stevenson, MM
研究了调理素非依赖性巨噬细胞吞噬作用作为控制早期血液期查鲍迪疟原虫感染的可能机制。在感染早期，耐药C57BL/6(B6)小鼠的腹腔巨噬细胞对寄生红细胞(PRBC)和游离裂殖子的吞噬能力增强，而干扰素-γ产生缺陷的小鼠(包括易感A/J、白介素12p40和干扰素-γ基因敲除小鼠)在感染过程中不存在这一现象。B6和A/J小鼠感染早期采集的巨噬细胞经干扰素-γ处理后，pRBC的吞噬功能增强，而IL-10处理则抑制这一功能。利用A类清道夫受体缺陷小鼠以及清道夫受体和甘露糖受体的抑制剂进行的体内外研究表明，除A类清道夫受体和甘露糖受体外，清道夫受体可能在疟疾寄生虫的摄取中起作用。这些结果表明，调理素非依赖性的吞噬作用有助于对急性血液期疟疾感染的干扰素-γ依赖的控制。
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.