衰老会延迟小鼠急性炎症的消退：用新型纳米促消退药物重编程宿主反应。
Aging delays resolution of acute inflammation in mice: reprogramming the host response with novel nano-proresolving medicines.
作者信息
Arnardottir Hildur H, Dalli Jesmond, Colas Romain A, Shinohara Masakazu, Serhan Charles N
机构信息
Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Harvard Institutes of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115.
Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Harvard Institutes of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115
出版信息
J Immunol. 2014 Oct 15;193(8):4235-44. doi: 10.4049/jimmunol.1401313. Epub 2014 Sep 12.
Aging is associated with an overt inflammatory phenotype and physiological decline. Specialized proresolving lipid mediators (SPMs) are endogenous autacoids that actively promote resolution of inflammation. In this study, we investigated resolution of acute inflammation in aging and the roles of SPMs. Using a self-resolving peritonitis and resolution indices coupled with lipid mediator metabololipidomics, we found that aged mice had both delayed resolution and reduced SPMs. The SPM precursor docosahexaenoic acid accelerated resolution via increased SPMs and promoted human monocyte reprogramming. In aged mice, novel nano-proresolving medicines carrying aspirin-triggered resolvins D1 and D3 reduced inflammation by promoting efferocytosis. These findings provide evidence for age-dependent resolution pathways in acute inflammation and novel means to activate resolution.
衰老与明显的炎症表型和生理衰退相关。特殊的促消退脂质介质（SPM）是内源性自分泌物质，可积极促进炎症的消退。在本研究中，我们调查了衰老过程中急性炎症的消退情况以及SPM的作用。通过一种自我消退的腹膜炎和消退指数，结合脂质介质代谢脂质组学，我们发现老年小鼠的炎症消退延迟且SPM减少。SPM前体二十二碳六烯酸通过增加SPM加速炎症消退，并促进人类单核细胞重编程。在老年小鼠中，携带阿司匹林触发的消退素D1和D3的新型纳米促消退药物通过促进胞葬作用减轻炎症。这些发现为急性炎症中年龄依赖性的消退途径提供了证据，并为激活炎症消退提供了新方法。
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