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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Opposing regulation of neutrophil apoptosis through the formyl peptide receptor-like 1/lipoxin A4 receptor: implications for resolution of inflammation.
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Opposing regulation of neutrophil apoptosis through the formyl peptide receptor-like 1/lipoxin A4 receptor: implications for resolution of inflammation.

机译：通过甲酰肽受体样1 /脂蛋白A4受体对嗜中性粒细胞凋亡的调节相反：对炎症消退的影响。

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摘要

Neutrophils have a central role in innate immunity, and their programmed cell death and removal are critical to the optimal expression as well as to efficient resolution of inflammation. Human neutrophils express the pleiotropic receptor formyl peptide receptor-like 1/lipoxin A4 (LXA(4)) receptor that binds a variety of ligands, including the acute-phase reactant serum amyloid A (SAA), the anti-inflammatory lipids LXA(4) and aspirin-triggered 15-epi-LXA(4) (ATL), and the glucocorticoid-inducible protein annexin 1. In addition to regulation of neutrophil activation and recruitment, these ligands have a profound influence on neutrophil survival and apoptosis with contrasting actions, mediating aggravation or resolution of the inflammatory response. Thus, annexin 1 accelerates, whereas SAA rescues human neutrophils from constitutive apoptosis by preventing mitochondrial dysfunction and subsequent activation of caspase-3. Furthermore, ATL overcomes the antiapoptosis signal from SAA and redirects neutrophils to caspase-mediated cell death. We review recent developments about the molecular basis of these actions and suggest a novel mechanism by which aspirin promotes resolution of acute inflammation and tissue injury.
机译：中性粒细胞在先天免疫中起着核心作用，它们的程序性细胞死亡和清除对于最佳表达以及有效解决炎症至关重要。人类嗜中性粒细胞表达与多种配体结合的多效性受体甲酰肽受体样1 /脂蛋白A4（LXA（4））受体，包括急性期反应物血清淀粉样蛋白A（SAA），抗炎脂质LXA（4） ）和阿司匹林触发的15-epi-LXA（4）（ATL）以及糖皮质激素诱导的蛋白Annexin1。除了调节嗜中性粒细胞的活化和募集外，这些配体还通过对比作用对嗜中性粒细胞的存活和凋亡产生深远影响介导炎症反应的加剧或消退。因此，膜联蛋白1加速，而SAA通过防止线粒体功能障碍和随后的caspase-3活化，使人类中性粒细胞免于组成性凋亡。此外，ATL克服了SAA的抗凋亡信号，并将中性粒细胞重新定向到caspase介导的细胞死亡。我们回顾了有关这些作用的分子基础的最新进展，并提出了一种新的机制，通过这种机制，阿司匹林可促进急性炎症和组织损伤的解决。

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