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本文引用的文献

1
Exhaled breath condensate eicosanoid levels associate with asthma and its severity.呼出气冷凝物中类二十烷酸水平与哮喘及其严重程度相关。
J Allergy Clin Immunol. 2013 Sep;132(3):547-553. doi: 10.1016/j.jaci.2013.01.058. Epub 2013 Apr 19.
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15-Epi-lipoxin A4 inhibits human neutrophil superoxide anion generation by regulating polyisoprenyl diphosphate phosphatase 1.15-Epi-脂氧素 A4 通过调节多萜醇二磷酸磷酸酶 1 抑制人中性粒细胞超氧阴离子生成。
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The novel 13S,14S-epoxy-maresin is converted by human macrophages to maresin 1 (MaR1), inhibits leukotriene A4 hydrolase (LTA4H), and shifts macrophage phenotype.新型 13S,14S-环氧马尿酸被人巨噬细胞转化为马尿酸 1(MaR1),抑制白三烯 A4 水解酶(LTA4H),并改变巨噬细胞表型。
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Lipoxin A4 regulates natural killer cell and type 2 innate lymphoid cell activation in asthma.脂氧素 A4 调节哮喘中自然杀伤细胞和 2 型先天淋巴细胞的激活。
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Resolvin D3 and aspirin-triggered resolvin D3 are potent immunoresolvents.消退素D3和阿司匹林触发的消退素D3是强效免疫溶解剂。
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Resolvin D2 restores neutrophil directionality and improves survival after burns.解析度 D2 可恢复中性粒细胞的定向迁移能力,并改善烧伤后的存活率。
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Anti-inflammatory therapy in chronic disease: challenges and opportunities.慢性病的抗炎治疗:挑战与机遇。
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Stereochemical assignment and anti-inflammatory properties of the omega-3 lipid mediator resolvin E3.立体化学分配和抗炎特性的 omega-3 脂质介质分辨率 E3。
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Microfluidic chambers for monitoring leukocyte trafficking and humanized nano-proresolving medicines interactions.用于监测白细胞迁移和人源化纳米分辨率药物相互作用的微流控室。
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Anti-inflammatory lipoxin A4 is an endogenous allosteric enhancer of CB1 cannabinoid receptor.抗炎性脂质素 A4 是 CB1 大麻素受体的内源性变构增强剂。
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肺部急性炎症的消退。

Resolution of acute inflammation in the lung.

机构信息

Pulmonary and Critical Care Medicine, Department of Internal Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115; email:

出版信息

Annu Rev Physiol. 2014;76:467-92. doi: 10.1146/annurev-physiol-021113-170408. Epub 2013 Dec 2.

DOI:10.1146/annurev-physiol-021113-170408
PMID:24313723
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4295924/
Abstract

Acute inflammation in the lung is essential to health. So too is its resolution. In response to invading microbes, noxious stimuli, or tissue injury, an acute inflammatory response is mounted to protect the host. To limit inflammation and prevent collateral injury of healthy, uninvolved tissue, the lung orchestrates the formation of specialized proresolving mediators, specifically lipoxins, resolvins, protectins, and maresins. These immunoresolvents are agonists for resolution that interact with specific receptors on leukocytes and structural cells to blunt further inflammation and promote catabasis. This process appears to be defective in several common lung diseases that are characterized by excess or chronic inflammation. Here, we review the molecular and cellular effectors of resolution of acute inflammation in the lung.

摘要

肺部的急性炎症对于健康至关重要。其消退也是如此。为了应对入侵的微生物、有害刺激物或组织损伤,会引发急性炎症反应来保护宿主。为了限制炎症并防止健康的未受影响的组织受到牵连性损伤,肺部会协调形成专门的促解决介质,特别是脂氧素、解析素、保护素和maresins。这些免疫调节剂是炎症消退的激动剂,与白细胞和结构细胞上的特定受体相互作用,以减弱进一步的炎症并促进衰退。这一过程似乎在几种常见的肺部疾病中存在缺陷,这些疾病的特征是过度或慢性炎症。在这里,我们回顾了肺部急性炎症消退的分子和细胞效应物。