Lack of Clinical Benefit of Interferon β-1a Among Patients With Severe Acute Respiratory Distress Syndrome: Time to Overhaul Drug Trials in ARDS?

TY - JOUR

T1 - Lack of Clinical Benefit of Interferon β-1a Among Patients With Severe Acute Respiratory Distress Syndrome: Time to Overhaul Drug Trials in ARDS?

AU - Shankar-Hari, Manu

AU - Calfee, Carolyn S.

PY - 2020/2/25

Y1 - 2020/2/25

N2 - 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. 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.

AB - 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. 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.

UR - http://www.scopus.com/inward/record.url?scp=85079645343&partnerID=8YFLogxK

U2 - 10.1001/jama.2019.22524

DO - 10.1001/jama.2019.22524

M3 - Editorial

SN - 0098-7484

VL - 323

SP - 713

EP - 715

JO - JAMA

JF - JAMA

IS - 8

ER -