Plasmodium yoelii blood-stage primes macrophage-mediated innate immune response through modulation of toll-like receptor signalling.
Plasmodium yoelii blood-stage primes macrophage-mediated innate immune response through modulation of toll-like receptor signalling.
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约氏疟原虫血期通过调节 Toll 样受体信号传导引发巨噬细胞介导的先天免疫反应
DOI：
10.1186/1475-2875-11-104
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发表时间：
2012-04-01
期刊：
影响因子：
3
通讯作者：
Xu W
中科院分区：
文献类型：
--
作者：
Fu Y;Ding Y;Zhou T;Fu X;Xu W
研究背景Toll样受体（Toll-like receptor，TLR）信号转导被恶性疟原虫（Plasmodiumfalciparum）激活。然而，很少有人知道的调节巨噬细胞TLR信号的感染致死或非致死菌株的啮齿类疟疾parasitis.MethodsBALB/c小鼠感染非致死strainPlasmodiumyoeli 17 XNL或致死strainP。yoeli17XL。分离小鼠腹腔巨噬细胞，研究其对pRBC裂解液和TLRs（TLR 2、TLR 4和TLR 9）激动剂的免疫应答，并通过流式细胞术和半定量RT-PCR检测TLRs和细胞内信号分子的表达。y17 XL或非致死菌株P.在感染后1、3和5天，y17 XNL对pRBC裂解物以及TLR 2、TLR 4和TLR 9激动剂增强。在所有测试的TLR中，只有TLR 2在感染任一菌株的小鼠的腹腔巨噬细胞上上调。然而，细胞内信号分子MyD 88，IRAK-1和TRAF-6的转录在感染P. yoeli 17 XL或P.感染后1、3和5天的yoeli 17 XNL。但P.感染约氏17 XNL的小鼠比感染P.结论P.约氏17 XL和17 XNL菌株可通过上调TLR 2和细胞内信号分子MyD 88、IRAK-1和TRAF-6的表达来增强腹腔巨噬细胞对pRBC裂解物和TLR激动剂的反应。此外，还可延长巨噬细胞对P.感染约氏17 XNL的小鼠可能与更有效地控制P.小鼠早期约氏17 XNL生长。
BackgroundToll-like receptors (TLRs) signalling is reported to be primed by the infection of human malaria parasite,Plasmodium falciparum. However, little is known about the regulation of macrophages TLR signalling by the infection of lethal or non-lethal strain of rodent malaria parasites.MethodsBALB/c mice were infected with non-lethal strainPlasmodium yoelii17XNL or lethal strainP. yoelii17XL. Peritoneal macrophages were isolated to study its immune response to pRBC lysate, and TLRs (TLR2, TLR4, and TLR9) agonists, and the expression of TLRs and intracellular signalling molecules were also investigated by flow cytometry and semi-quantitive RT-PCR.ResultsThe reactivity of peritoneal macrophages from the mice infected with lethal strainP. y17XL or non-lethal strainP. y17XNL were enhanced to pRBC lysate, and TLR2, TLR4, and TLR9 agonists at one, three and five days post-infection. Of all the tested TLRs, only TLR2 was up-regulated on peritoneal macrophages of mice infected with either strain. However, transcription of intracellular signalling molecules MyD88, IRAK-1, and TRAF-6 was significantly up-regulated in peritoneal macrophages from mice infected either withP. yoelii17XL orP. yoelii17XNL at one, three and five days post-infection. However, the enhanced TLRs response of macrophage fromP. yoelii17XNL-infected mice persisted for a much longer time than that fromP. yoelii17XL-infected mice.ConclusionBothP. yoelii17XL and 17XNL strains could enhance the response of peritoneal macrophages to pRBC lysate and TLR agonists, through up-regulating the expression of TLR2 and intracellular signalling molecules MyD88, IRAK-1, and TRAF-6. In addition, prolonged high response of macrophage fromP. yoelii17XNL-infected mice might be associated with the more efficiently controlling ofP. yoelii17XNL growth in mice at early stage.
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DOI：
10.1084/jem.20041836
发表时间：
2005-01-03
期刊：
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影响因子：
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发表时间：
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