| First Author | Felton JM | Year | 2020 |
| Journal | Thorax | Volume | 75 |
| Issue | 7 | Pages | 600-605 |
| PubMed ID | 32303624 | Mgi Jnum | J:293652 |
| Mgi Id | MGI:6453153 | Doi | 10.1136/thoraxjnl-2019-213204 |
| Citation | Felton JM, et al. (2020) Mcl-1 protects eosinophils from apoptosis and exacerbates allergic airway inflammation. Thorax 75(7):600-605 |
| abstractText | 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. |
