RT Journal Article SR Electronic T1 The cyclin-dependent kinase inhibitor AT7519 accelerates neutrophil apoptosis in sepsis-related acute respiratory distress syndrome JF Thorax JO Thorax FD BMJ Publishing Group Ltd and British Thoracic Society SP 182 OP 185 DO 10.1136/thoraxjnl-2016-209229 VO 72 IS 2 A1 David A Dorward A1 Jennifer M Felton A1 Calum T Robb A1 Thomas Craven A1 Tiina Kipari A1 Timothy S Walsh A1 Christopher Haslett A1 Kallirroi Kefala A1 Adriano G Rossi A1 Christopher D Lucas YR 2017 UL http://thorax.bmj.com/content/72/2/182.abstract AB Acute respiratory distress syndrome (ARDS) is a neutrophil-dominant disorder with no effective pharmacological therapies. While the cyclin-dependent kinase inhibitor AT7519 induces neutrophil apoptosis to promote inflammation resolution in preclinical models of lung inflammation, its potential efficacy in ARDS has not been examined. Untreated peripheral blood sepsis-related ARDS neutrophils demonstrated prolonged survival after 20 hours in vitro culture. AT7519 was able to override this phenotype to induce apoptosis in ARDS neutrophils with reduced expression of the pro-survival protein Mcl-1. We demonstrate the first pharmacological compound to induce neutrophil apoptosis in sepsis-related ARDS, highlighting cyclin-dependent kinase inhibitors as potential novel therapeutic agents.