Disease: correlates of protection, determinants of outcome and clinical management' amended to incorporate urgent COVID-19 studies and contract number 75F40120C00085 'Characterization of severe coronavirus infection in humans and model systems for medical countermeasure development and evaluation' awarded to
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.
Pulmonary microthrombosis and vasculitis occur in fatal coronavirus disease 2019. To determine whether these processes occur in other life-threatening respiratory virus infections, we identified autopsy studies of fatal influenza (n = 455 patients), severe acute respiratory syndrome ([SARS] n = 37), Middle East respiratory syndrome (n = 2), adenovirus (n = 34), and respiratory syncytial virus (n = 30). Histological evidence of thrombosis was frequently present in adults with fatal influenza and SARS, with vasculitis also reported.
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