Specialized pro-resolving mediators: endogenous regulators of infection and inflammation.

Specialized pro-resolving mediators: endogenous regulators of infection and inflammation.
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专门的促解决介质:感染和炎症的内源性调节剂。

DOI:
10.1038/nri.2015.4
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发表时间:
2016-01
期刊:
Nature reviews. Immunology
影响因子:
--
通讯作者:
Levy BD
Levy BD
中科院分区:
其他
文献类型:
--
作者:
Basil MC;Levy BD

文献摘要

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免疫应答不仅包括促炎和抗炎途径,还包括促消退机制,其用于平衡宿主对靶向微生物病原体的需要,同时防止过度炎症和旁观者组织损伤。特异性促消退介质(SPMs)是酶促衍生自必需脂肪酸的一类新型免疫消退剂,其限制急性反应并协调组织病原体、垂死细胞和感染性炎症战场碎片的清除。SPM由脂氧素、E系列和D系列消退素、保护素和maresins组成。SPM家族的单个成员作为同源受体的激动剂诱导细胞类型特异性反应。SPMs在宿主对细菌、病毒、真菌和寄生虫病原体等多种微生物的应答中发挥着重要的调节作用。SPM还促进非感染性炎症和组织损伤的解决。宿主SPM通路的缺陷有助于慢性炎性疾病的发展。由于能够增强宿主防御和调节炎症,SPM代表了一种有前途的翻译方法,以争取宿主解决方案用于治疗感染和过度炎症。本文的在线版本(doi:10.1038/nri.2015.4)包含补充材料,可供授权用户使用。在这里,作者详细介绍了我们目前对专业促消退介质(SPM)的理解,这是一个内源性介质家族,在促进炎症消退方面发挥重要作用。以肺部为重点,他们讨论了SPM对感染性和慢性炎症性疾病的贡献及其新兴的治疗潜力。本文的在线版本(doi:10.1038/nri.2015.4)包含补充材料,可供授权用户使用。专门的促消退介质(SPM)是酶促衍生自必需脂肪酸,并在协调组织炎症消退(即缓解)中发挥重要作用。宿主对组织感染的反应引起急性炎症,试图控制入侵的病原体。SPM是脂质介质,是一个更大的促分解分子家族的一部分,包括蛋白质和气体,它们共同抑制炎症并解决感染。这些免疫溶解剂与免疫抑制分子不同,因为它们不仅抑制炎症,而且促进宿主防御。在这里,我们主要关注SPM及其在肺部感染和炎症中的作用,以说明这些介质在感染后恢复组织稳态中的有效作用。本文的在线版本(doi:10.1038/nri.2015.4)包含补充材料,可供授权用户使用。
The immune response comprises not only pro-inflammatory and anti-inflammatory pathways but also pro-resolution mechanisms that serve to balance the need of the host to target microbial pathogens while preventing excess inflammation and bystander tissue damage. Specialized pro-resolving mediators (SPMs) are enzymatically derived from essential fatty acids to serve as a novel class of immunoresolvents that limit acute responses and orchestrate the clearance of tissue pathogens, dying cells and debris from the battlefield of infectious inflammation. SPMs are composed of lipoxins, E-series and D-series resolvins, protectins and maresins. Individual members of the SPM family serve as agonists at cognate receptors to induce cell-type specific responses. Important regulatory roles for SPMs have been uncovered in host responses to several microorganisms, including bacterial, viral, fungal and parasitic pathogens. SPMs also promote the resolution of non-infectious inflammation and tissue injury. Defects in host SPM pathways contribute to the development of chronic inflammatory diseases. With the capacity to enhance host defence and modulate inflammation, SPMs represent a promising translational approach to enlist host resolution programmes for the treatment of infection and excess inflammation. The online version of this article (doi:10.1038/nri.2015.4) contains supplementary material, which is available to authorized users. Here, the authors detail our current understanding of specialized pro-resolving mediators (SPMs), a family of endogenous mediators that have important roles in promoting the resolution of inflammation. With a focus on the lungs, they discuss the contribution of SPMs to infectious and chronic inflammatory diseases and their emerging therapeutic potential. The online version of this article (doi:10.1038/nri.2015.4) contains supplementary material, which is available to authorized users. Specialized pro-resolving mediators (SPMs) are enzymatically derived from essential fatty acids and have important roles in orchestrating the resolution of tissue inflammation — that is, catabasis. Host responses to tissue infection elicit acute inflammation in an attempt to control invading pathogens. SPMs are lipid mediators that are part of a larger family of pro-resolving molecules, which includes proteins and gases, that together restrain inflammation and resolve the infection. These immunoresolvents are distinct from immunosuppressive molecules as they not only dampen inflammation but also promote host defence. Here, we focus primarily on SPMs and their roles in lung infection and inflammation to illustrate the potent actions these mediators play in restoring tissue homeostasis after an infection. The online version of this article (doi:10.1038/nri.2015.4) contains supplementary material, which is available to authorized users.