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纤维蛋白原样蛋白 2 通过与分辨率素 Dp5 相互作用控制脓毒症消退。

Fibrinogen-like protein 2 controls sepsis catabasis by interacting with resolvin Dp5.

机构信息

Clinical Medicine Research Center, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China.

Institute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China.

出版信息

Sci Adv. 2019 Nov 13;5(11):eaax0629. doi: 10.1126/sciadv.aax0629. eCollection 2019 Nov.

DOI:10.1126/sciadv.aax0629
PMID:31763448
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6853772/
Abstract

The mechanisms that drive programmed resolution of inflammation remain elusive. Here, we report the temporal regulation of soluble (s) and transmembrane (m) fibrinogen-like protein 2 (Fgl2) during inflammation and show that both sFgl2 and mFgl2 correlate with the outcome. The expression and ectodomain shedding of Fgl2 are respectively promoted by miR-466l and metalloproteinases (ADAM10 and ADAM17) during inflammation resolution. Deficiency of Fgl2 enhances polymorphonuclear neutrophil (PMN) infiltration but impairs macrophage (MΦ) maturation and phagocytosis and inhibits the production of n-3 docosapentaenoic acid-derived resolvin 5 (RvDp5). In contrast, administration of sFgl2 blunts PMN infiltration as well as promotes PMN apoptosis and RvDp5 biosynthesis. By activating ALX/FPR2, RvDp5 enhances sFgl2 secretion via ADAM17 and synergistically accelerates resolution of inflammation. These results uncover a previously unknown endogenous programmed mechanism by which Fgl2 regulates resolution of inflammation and shed new light on clinical sepsis treatments.

摘要

驱动炎症程序性消退的机制仍然难以捉摸。在这里，我们报告了可溶性（s）和跨膜（m）纤维蛋白原样蛋白 2（Fgl2）在炎症过程中的时间调节，并表明 sFgl2 和 mFgl2 均与结果相关。在炎症消退过程中，miR-466l 和金属蛋白酶（ADAM10 和 ADAM17）分别促进 Fgl2 的表达和胞外结构域脱落。Fgl2 缺陷增强多形核粒细胞（PMN）浸润，但损害巨噬细胞（MΦ）成熟和吞噬作用，并抑制 n-3 二十二碳五烯酸衍生的分辨率 5（RvDp5）的产生。相比之下，sFgl2 的给药会削弱 PMN 的浸润，并促进 PMN 的凋亡和 RvDp5 的生物合成。通过激活 ALX/FPR2，RvDp5 通过 ADAM17 激活 sFgl2 分泌，并协同加速炎症消退。这些结果揭示了一种以前未知的内源性程序性机制，Fgl2 通过该机制调节炎症消退，并为临床败血症治疗提供了新的思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/387d/6853772/d4d31abf92c6/aax0629-F6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/387d/6853772/bbbaf52e4ca9/aax0629-F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/387d/6853772/2b088776e856/aax0629-F2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/387d/6853772/b08ee5abc856/aax0629-F4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/387d/6853772/8fd59a13f1a3/aax0629-F5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/387d/6853772/d4d31abf92c6/aax0629-F6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/387d/6853772/bbbaf52e4ca9/aax0629-F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/387d/6853772/2b088776e856/aax0629-F2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/387d/6853772/b08ee5abc856/aax0629-F4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/387d/6853772/8fd59a13f1a3/aax0629-F5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/387d/6853772/d4d31abf92c6/aax0629-F6.jpg

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