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Lysophosphatidylglycerol inhibits formyl peptide receptor like-1-stimulated chemotactic migration and IL-1β production from human phagocytes

机译:溶血磷脂酰甘油抑制人吞噬细胞像甲1刺激的趋化迁移和IL-1β产生的甲酰肽受体

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摘要

In this study, we observed that lysophosphatidylglycerol (LPG) completely inhibited a formyl peptide receptor like-1 (FPRL1) agonist (MMK-1)-stimulated chemotactic migration in human phagocytes, such as neutrophils and monocytes. LPG also dramatically inhibited IL-1β production by another FPRL1 agonist serum amyloid A (SAA) in human phagocytes. However, LPG itself induced intracellular calcium increase and superoxide anion production in human phagocytes. Keeping in mind that phagocytes migration and IL-1β production by FPRL1 are important for the induction of inflammatory response, our data suggest that LPG can be regarded as a useful material for the modulation of inflammatory response induced by FPRL1 activation.
机译:在这项研究中,我们观察到溶血磷脂酰甘油(LPG)完全抑制了人类吞噬细胞(如中性粒细胞和单核细胞)中甲酰肽受体样1(FPRL1)激动剂(MMK-1)刺激的趋化性迁移。 LPG还可显着抑制人吞噬细胞中另一种FPRL1激动剂血清淀粉样蛋白A(SAA)产生的IL-1β。但是,LPG本身会引起人类吞噬细胞中细胞内钙的增加和超氧阴离子的产生。请记住,FPRL1吞噬细胞迁移和IL-1β的产生对于诱导炎症反应很重要,我们的数据表明LPG可以被视为调节FPRL1激活诱导的炎症反应的有用物质。

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