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首页> 外文期刊>Toxicology Letters: An International Journal Providing a Forum for Original and Pertinent Contributions in Toxicology Research >Lipopolysaccharide triggers macrophage activation of inflammatory cytokine expression, chemotaxis, phagocytosis, and oxidative ability via a toll-like receptor 4-dependent pathway: Validated by RNA interference
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Lipopolysaccharide triggers macrophage activation of inflammatory cytokine expression, chemotaxis, phagocytosis, and oxidative ability via a toll-like receptor 4-dependent pathway: Validated by RNA interference

机译：脂多糖触发巨噬细胞激活炎症细胞因子表达，趋化性的受体4依赖性途径：通过RNA干扰验证

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摘要

RNA interference has been extensively used to knock-down the translation of certain genes. Toll-like receptor 4 (TLR4) produced by macrophages can be activated in response to endotoxin stimulation. This study used the RNA interference technique to evaluate the roles of TLR4 in lipopolysaccharide (LPS)-stimulated activation of macrophages from the aspects of cytokine production, chemotaxis, phagocytosis, and oxidative ability. Exposure of macrophages to 1,25,50,100 ng/mL LPS for 1,6, and 24 h did not affect cell viability. Meanwhile, treatment with 100 ng/mL LPS induced interleukin (IL)-l beta protein and mRNA syntheses in a time-dependent manner. Application of TLR4 small interference (si)RNA into macrophages decreased the levels of this receptor, and simultaneously ameliorated LPS-induced IL-1 betaand 1L-6 mRNA production. Transwell analysis showed that LPS increased chemotactic activity of macrophages, but application of TLR4 siRNA reduced such an effect. Phagocytic activities of macrophages were significantly augmented following LPS treatment. However, knocking-down the translation of TLR4 mRNA using RNA interference lowered the LPS-enhanced phagocytic activity. Analysis of flow cytometry revealed that LPS increased oxidative ability of macrophages, but TLR4 siRNA inhibited such development. This study used RNA interference techniques to show that TLR4 can mediate LPS-induced macrophage activations of IL-1 beta and IL-6 gene expression, chemotaxis, phagocytosis, and oxidative ability.
机译：RNA干扰已被广泛地用于击倒某些基因的翻译。通过巨噬细胞产生的Toll样受体4（TLR4）可以响应于内毒素刺激而被激活。该研究使用RNA干扰技术从细胞因子生产，趋化性，吞噬作用和氧化能力的方面评估TLR4在脂多糖（LPS）纯化活化的角色的作用。暴露于巨噬细胞至1,25,50,100ng / ml LPS，1,6和24小时不影响细胞活力。同时，用100ng / ml Lps诱导白细胞介素（IL）-Lβ蛋白和mRNA以时间依赖性方式处理。将TLR4小的干扰（Si）RNA施用于巨噬细胞下降，降低了该受体的水平，同时改善了LPS诱导的IL-1β和1L-6 mRNA产生。 Transwell分析表明，LPS增加了巨噬细胞的趋化活性，但在TLR4 siRNA的应用降低了这种效果。在LPS治疗后，巨噬细胞的吞噬活动显着增强。然而，使用RNA干扰敲击TLR4 mRNA的翻译降低了LPS增强的吞噬活性。流式细胞仪的分析显示，LPS增加巨噬细胞的氧化能力，但TLR4 siRNA抑制这种发展。该研究使用RNA干扰技术表明TLR4可以介导IL-1β和IL-6基因表达，趋化性，吞噬作用和氧化能力的LPS诱导的巨噬细胞激活。

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