TY - JOUR T1 - Mcl-1 protects eosinophils from apoptosis and exacerbates allergic airway inflammation JF - Thorax JO - Thorax SP - 600 LP - 605 DO - 10.1136/thoraxjnl-2019-213204 VL - 75 IS - 7 AU - Jennifer M Felton AU - David A Dorward AU - Jennifer A Cartwright AU - Philippe MD Potey AU - Calum T Robb AU - Jingang Gui AU - Ruth W Craig AU - Jürgen Schwarze AU - Christopher Haslett AU - Rodger Duffin AU - Ian Dransfield AU - Christopher D Lucas AU - Adriano G Rossi Y1 - 2020/07/01 UR - http://thorax.bmj.com/content/75/7/600.abstract N2 - 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. ER -