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首页> 外文期刊>Infection and immunity >Toxoplasma gondii Inhibits Toll-Like Receptor 4 Ligand-Induced Mobilization of Intracellular Tumor Necrosis Factor Alpha to the Surface of Mouse Peritoneal Neutrophils
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Toxoplasma gondii Inhibits Toll-Like Receptor 4 Ligand-Induced Mobilization of Intracellular Tumor Necrosis Factor Alpha to the Surface of Mouse Peritoneal Neutrophils

机译：弓形虫抑制Toll样受体4配体诱导的小鼠腹膜中性粒细胞表面细胞内肿瘤坏死因子α的动员。

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Neutrophils are well-known to rapidly respond to infection through chemotactic infiltration at sites of inflammation, followed by rapid release of microbicidal molecules, chemokines, and proinflammatory cytokines. For tumor necrosis factor alpha (TNF-α), we recently found that neutrophils contain intracellular pools of the cytokine and display the capacity to upregulate transcriptional activity of the gene during lipopolysaccharide (LPS) stimulation. We now show that triggering of mouse peritoneal neutrophils with Toll-like receptor 2 (TLR2), TLR4, and TLR9 ligands, but not ligands of TLR3, induces upregulation of surface membrane TNF-α. However, neutrophils infected with the protozoan Toxoplasma gondii displayed an inability to respond fully in terms of TLR ligand-induced increases in membrane TNF-α expression. Infected neutrophils failed to display decreased levels of intracellular TNF-α upon LPS exposure. In contrast to intermediate inhibitory effects in nontreated neutrophils, T. gondii induced a complete blockade in LPS-induced surface TNF-α expression in the presence of the protein synthesis inhibitor cycloheximide. Despite these inhibitory effects, the parasite did not affect LPS-induced upregulation of TNF-α gene transcription. Collectively, the results show that Toxoplasma prevents TLR ligand-triggered mobilization of TNF-α to the neutrophil surface, revealing a novel immunosuppressive activity of the parasite.
机译：众所周知，嗜中性粒细胞可通过炎症部位的趋化渗透迅速响应感染，然后迅速释放杀菌分子，趋化因子和促炎细胞因子。对于肿瘤坏死因子α（TNF-α），我们最近发现嗜中性粒细胞含有细胞因子的细胞内池，并在脂多糖（LPS）刺激过程中显示出上调基因转录活性的能力。我们现在显示，用Toll样受体2（TLR2），TLR4和TLR9配体而非TLR3的配体触发小鼠腹膜中性粒细胞诱导表面膜TNF-α的上调。但是，感染了原生动物弓形虫的嗜中性粒细胞不能完全响应TLR配体诱导的膜TNF-α表达的增加。 LPS暴露后，感染的中性粒细胞未能显示出降低的细胞内TNF-α水平。与未经处理的嗜中性粒细胞的中间抑制作用相反， T。在蛋白质合成抑制剂环己酰亚胺的存在下，gondii 完全阻断了LPS诱导的表面TNF-α表达。尽管有这些抑制作用，该寄生虫仍不影响LPS诱导的TNF-α基因转录的上调。总体而言，结果表明，弓形虫阻止了TLR配体触发的TNF-α向中性粒细胞表面的动员，从而揭示了该寄生虫的新型免疫抑制活性。

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