Mcl-1 protects eosinophils from apoptosis and exacerbates allergic airway inflammation

Jennifer M Felton, David A Dorward, Jennifer Cartwright, Philippe M D Potey, Calum T Robb, Jingang Gui, Ruth W Craig, Jurgen Schwarze, Christopher Haslett, Rodger Duffin, Ian Dransfield, Christopher D Lucas, Adriano G Rossi

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

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 Mcl-1 mice (hMcl-1) and reducing Mcl-1 by a cyclin-dependent kinase inhibitor.
Over-expression 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.
Original languageEnglish
Pages (from-to)600-605
Issue number7
Early online date17 Apr 2020
Publication statusPublished - 1 Jul 2020


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