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.
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。.
Keywords: Acute Lung Injury; Acute Respiratory Distress Syndrome; Alveolar Fluid Clearance; Specialized Pro-resolving Mediator.