In acute respiratory distress syndrome (ARDS), the alveolar-capillary units are disrupted, with lung endothelial and epithelial injury resulting in exudative pulmonary edema containing inflammatory mediators, solutes, proteins, and leukocytes.¹ Treating pulmonary endothelial injury in ARDS may improve patient outcomes. Interferon β-1a (IFN-β-1a), a type 1 IFN, is one such treatment that may improve pulmonary endothelial barrier function. In addition to its myriad immunologic effects, IFN-β-1a upregulates cluster of differentiation 73 (CD73) on pulmonary endothelial cells, thereby increasing extracellular adenosine concentrations, which acting via adenosine receptors improves pulmonary endothelial barrier function through junctional reorganization, cytoskeleton rearrangement, and further transcriptional upregulation of CD73.^2-4

在急性呼吸窘迫综合征（ARDS）中，肺泡-毛细血管单位被破坏，肺内皮和上皮受到损伤，导致渗出性肺水肿，其中包含炎性介质，溶质，蛋白质和白细胞。^1个治疗ARDS中的肺内皮损伤可改善患者预后。干扰素β-1a（IFN-β-1a）是一种1型干扰素，可以改善肺血管内皮屏障功能。除具有无数的免疫作用外，IFN-β-1a还上调了肺血管内皮细胞的分化簇73（CD73），从而增加了细胞外腺苷的浓度，这些腺苷通过腺苷受体起作用，可通过连接重组，细胞骨架重排和增强肺内皮屏障功能。 CD73进一步转录上调。^{2 -4}