RT Journal Article SR Electronic T1 Mcl-1 protects eosinophils from apoptosis and exacerbates allergic airway inflammation JF Thorax JO Thorax FD BMJ Publishing Group Ltd and British Thoracic Society SP 600 OP 605 DO 10.1136/thoraxjnl-2019-213204 VO 75 IS 7 A1 Jennifer M Felton A1 David A Dorward A1 Jennifer A Cartwright A1 Philippe MD Potey A1 Calum T Robb A1 Jingang Gui A1 Ruth W Craig A1 Jürgen Schwarze A1 Christopher Haslett A1 Rodger Duffin A1 Ian Dransfield A1 Christopher D Lucas A1 Adriano G Rossi YR 2020 UL http://thorax.bmj.com/content/75/7/600.abstract AB Eosinophils are key effector cells in allergic diseases. Here we investigated Mcl-1 (an anti-apoptotic protein) in experimental allergic airway inflammation using transgenic overexpressing human Mcl-1 mice (hMcl-1) and reducing Mcl-1 by a cyclin-dependent kinase inhibitor. Overexpression of Mcl-1 exacerbated allergic airway inflammation, with increased bronchoalveolar lavage fluid cellularity, eosinophil numbers and total protein, and an increase in airway mucus production. Eosinophil apoptosis was suppressed by Mcl-1 overexpression, with this resistance to apoptosis attenuated by cyclin-dependent kinase inhibition which also rescued Mcl-1-exacerbated allergic airway inflammation. We propose that targeting Mcl-1 may be beneficial in treatment of allergic airway disease.