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
Shankar-Hari M, Calfee CS. Lack of Clinical Benefit of Interferon β-1a Among Patients With Severe Acute Respiratory Distress Syndrome: Time to Overhaul Drug Trials in ARDS? JAMA. 2020;323(8):713–715. doi:10.1001/jama.2019.22524
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