急性炎症期间脂质介质类别转换：炎症消退中的信号
Lipid mediator class switching during acute inflammation: signals in resolution.
作者信息
Levy B D, Clish C B, Schmidt B, Gronert K, Serhan C N
机构信息
Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA.
出版信息
Nat Immunol. 2001 Jul;2(7):612-9. doi: 10.1038/89759.
Leukotrienes (LTs) and prostaglandins (PGs) amplify acute inflammation, whereas lipoxins (LXs) have unique anti-inflammatory actions. Temporal analyses of these eicosanoids in clinical and experimental exudates showed early coordinate appearance of LT and PG with polymorphonuclear neutrophil (PMN) recruitment. This was followed by LX biosynthesis, which was concurrent with spontaneous resolution. Human peripheral blood PMNs exposed to PGE2 (as in exudates) switched eicosanoid biosynthesis from predominantly LTB4 and 5-lipoxygenase (5-LO)-initiated pathways to LXA4, a 15-LO product that "stopped" PMN infiltration. These results indicate that first-phase eicosanoids promote a shift to anti-inflammatory lipids: functionally distinct lipid-mediator profiles switch during acute exudate formation to "reprogram" the exudate PMNs to promote resolution.
白三烯（LTs）和前列腺素（PGs）会加剧急性炎症，而脂氧素（LXs）则具有独特的抗炎作用。对临床和实验性渗出液中这些类二十烷酸的时间分析显示，LT和PG与多形核中性粒细胞（PMN）募集同时早期出现。随后是LX生物合成，这与渗出液的自然消退同时发生。暴露于PGE2（如在渗出液中）的人外周血PMN将类二十烷酸生物合成从主要由LTB4和5-脂氧合酶（5-LO）启动的途径转变为LXA4，LXA4是一种15-LO产物，可“阻止”PMN浸润。这些结果表明，第一阶段的类二十烷酸会促进向抗炎脂质的转变：在急性渗出液形成过程中，功能不同的脂质介质谱会发生切换，以“重新编程”渗出液中的PMN以促进消退。
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