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Down Regulation of MyD88 in Macrophages Treated with Liposomes Composed of Phosphatidylserine

机译:磷脂酰丝氨酸脂质体处理巨噬细胞中MyD88的下调

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We have recently demonstrated that liposomes composed of phosphatidylserine (PS-liposomes) suppressed nitric oxide and inflammatory cytokine productions following LPS stimulation in macrophages. In this study, we examined the effect of PS-liposomes on expressions of TLR-4 and MyD88, which are essential for the signal transduction in LPS stimulation. Expression of MyD88 was suppressed when macrophages were treated with PS-liposomes, but not with liposomes of phosphatidylcholine. No change in TLR-4 expression was observed. MyD88 suppression was restored to the control levels when cells were pre-treated with anti-TGF-β antibody, suggesting that TGF-β plays an important role in down-regulation of MyD88 following PS-liposome treatment.
机译:我们最近证明,由磷脂酰丝氨酸组成的脂质体(PS-脂质体)可抑制巨噬细胞中LPS刺激后的一氧化氮和炎性细胞因子的产生。在这项研究中,我们检查了PS脂质体对TLR-4和MyD88表达的影响,这对于LPS刺激中的信号转导至关重要。当用PS脂质体而不是磷脂酰胆碱脂质体处理巨噬细胞时,MyD88的表达被抑制。没有观察到TLR-4表达的变化。当用抗TGF-β抗体预处理细胞后,MyD88抑制恢复到对照水平,表明TGF-β在PS脂质体处理后在MyD88的下调中起重要作用。

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