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      Specialized Pro-resolving Mediators Regulate Alveolar Fluid Clearance during Acute Respiratory Distress Syndrome Translated title: 促炎症消退介质调控急性呼吸窘迫综合征肺泡液体清除率的机制

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          Abstract

          Objective:

          Acute respiratory distress syndrome (ARDS) is an acute and lethal clinical syndrome that is characterized by the injury of alveolar epithelium, which impairs active fluid transport in the lung, and impedes the reabsorption of edema fluid from the alveolar space. This review aimed to discuss the role of pro-resolving mediators on the regulation of alveolar fluid clearance (AFC) in ARDS.

          Data Sources:

          Articles published up to September 2017 were selected from the PubMed, with the keywords of “alveolar fluid clearance” or “lung edema” or “acute lung injury” or “acute respiratory distress syndrome”, and “specialized pro-resolving mediators” or “lipoxin” or “resolvin” or “protectin” or “maresin” or “alveolar epithelial cells” or “aspirin-triggered lipid mediators” or “carbon monoxide and heme oxygenase” or “annexin A1”.

          Study Selection:

          We included all relevant articles published up to September 2017, with no limitation of study design.

          Results:

          Specialized pro-resolving mediators (SPMs), as the proinflammatory mediators, not only upregulated epithelial sodium channel, Na,K-ATPase, cystic fibrosis transmembrane conductance regulator (CFTR), and aquaporins levels, but also improved Na,K-ATPase activity to promote AFC in ARDS. In addition to the direct effects on ion channels and pumps of the alveolar epithelium, the SPMs also inhibited the inflammatory cytokine expression and improved the alveolar epithelial cell repair to enhance the AFC in ARDS.

          Conclusions:

          The present review discusses a novel mechanism for pulmonary edema fluid reabsorption. SPMs might provide new opportunities to design “reabsorption-targeted” therapies with high degrees of precision in controlling ALI/ARDS.

          摘要

          目的:

          急性呼吸窘迫综合征(ARDS)是一种临床急危重症,其主要特征是肺泡上皮损伤削弱肺内液体主动转运,限制水肿液从肺泡腔中重新吸收。本综述旨在探讨促炎症消退介质调控ARDS肺泡液清除(AFC)的机制。

          数据来源:

          截止2017年9月1日,所有发表在PubMed上的文章。查询关键词为:“alveolar fluid clearance”或“lung edema”或“acute lung injury”或“acute respiratory distress syndrome”和“specialized pro-resolving mediators”或“lipoxin”或“resolvin”或“protectin” 或“maresin”或“alveolar epithelial cells”或“aspirin-triggered lipid mediators”或“carbon monoxide and heme oxygenase”或“annexin A1”。

          研究选择:

          综述包含了截止2017年9月1日出版了的所有相关的文章,对研究设计无限制。

          结果:

          作为促炎症消退介质,SPMs不仅上调ENaC,Na,K-ATPase,囊性纤维化跨膜传导调节因子(CFTR)和水通道蛋白水平,而且增强Na,K-ATPase活性,进而促进ARDS中的AFC。SPMs除了直接影响肺泡上皮的离子通道和泵外,还能抑制炎症因子的表达,改善肺泡上皮细胞的修复功能,进一步增强ARDS的AFC。

          结论:

          本综述探讨了一种肺泡水肿液重吸收的新机制。SPMs可能为控制急性肺损伤(ALI)/ARDS提供高精确度的“重吸收靶向”治疗提供新的机会。

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          Most cited references79

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          Annexin A1 and glucocorticoids as effectors of the resolution of inflammation.

          Glucocorticoids are widely used for the management of inflammatory diseases. Their clinical application stems from our understanding of the inhibitory effect of the corticosteroid hormone cortisol on several components of the immune system. Endogenous and exogenous glucocorticoids mediate their multiple anti-inflammatory effects through many effector molecules. In this Opinion article, we focus on the role of one such effector molecule, annexin A1, and summarize the recent studies that provide insight into its molecular and pharmacological functions in immune responses. In addition, we propose a model in which glucocorticoids regulate the expression and function of annexin A1 in opposing ways in innate and adaptive immune cells to mediate the resolution of inflammation.
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            Amiloride-sensitive epithelial Na+ channel is made of three homologous subunits.

            The amiloride-sensitive epithelial sodium channel constitutes the rate-limiting step for sodium reabsorption in epithelial cells that line the distal part of the renal tubule, the distal colon, the duct of several exocrine glands, and the lung. The activity of this channel is upregulated by vasopressin and aldosterone, hormones involved in the maintenance of sodium balance, blood volume and blood pressure. We have identified the primary structure of the alpha-subunit of the rat epithelial sodium channel by expression cloning in Xenopus laevis oocytes. An identical subunit has recently been reported. Here we identify two other subunits (beta and gamma) by functional complementation of the alpha-subunit of the rat epithelial Na+ channel. The ion-selective permeability, the gating properties and the pharmacological profile of the channel formed by coexpressing the three subunits in oocytes are similar to that of the native channel.
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              • Article: found
              Is Open Access

              Maresins: novel macrophage mediators with potent antiinflammatory and proresolving actions

              The endogenous cellular and molecular mechanisms that control acute inflammation and its resolution are of wide interest. Using self-resolving inflammatory exudates and lipidomics, we have identified a new pathway involving biosynthesis of potent antiinflammatory and proresolving mediators from the essential fatty acid docosahexaenoic acid (DHA) by macrophages (MΦs). During the resolution of mouse peritonitis, exudates accumulated both 17-hydroxydocosahexaenoic acid, a known marker of 17S-D series resolvin (Rv) and protectin biosynthesis, and 14S-hydroxydocosa-4Z,7Z,10Z,12E,16Z,19Z-hexaenoic acid from endogenous DHA. Addition of either DHA or 14S-hydroperoxydocosa-4Z,7Z,10Z,12E,16Z,19Z-hexaenoic acid to activated MΦs converted these substrates to novel dihydroxy-containing products that possessed potent antiinflammatory and proresolving activity with a potency similar to resolvin E1, 5S,12R,18R-trihydroxyeicosa-6Z,8E,10E,14Z,16E-pentaenoic acid, and protectin D1, 10R,17S-dihydroxydocosa-4Z,7Z,11E,13E,15Z,19Z-hexaenoic acid. Stable isotope incorporation, intermediate trapping, and characterization of physical and biological properties of the products demonstrated a novel 14-lipoxygenase pathway, generating bioactive 7,14-dihydroxydocosa-4Z,8,10,12,16Z,19Z-hexaenoic acid, coined MΦ mediator in resolving inflammation (maresin), which enhances resolution. These findings suggest that maresins and this new metabolome may be involved in some of the beneficial actions of DHA and MΦs in tissue homeostasis, inflammation resolution, wound healing, and host defense.
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                Author and article information

                Journal
                Chin Med J (Engl)
                Chin. Med. J
                CMJ
                Chinese Medical Journal
                Medknow Publications & Media Pvt Ltd (India )
                0366-6999
                20 April 2018
                : 131
                : 8
                : 982-989
                Affiliations
                [1]Department of Anesthesia and Critical Care, Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China
                Author notes
                Address for correspondence: Dr. Sheng-Wei Jin, Department of Anesthesia and Critical Care, Second Affiliated Hospital of Wenzhou Medical University, 109 Xueyuan Road, Wenzhou, Zhejiang 325027, China E-Mail: jinshengwei69@ 123456163.com
                Article
                CMJ-131-982
                10.4103/0366-6999.229890
                5912066
                29664060
                5105b2ef-47d3-4e31-9ceb-d2d64160f7a2
                Copyright: © 2018 Chinese Medical Journal

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

                History
                : 23 October 2017
                Categories
                Review Article

                acute lung injury,acute respiratory distress syndrome,alveolar fluid clearance,specialized pro-resolving mediator

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