Author: Aran Singanayagam; Joseph Footitt; Benjamin T Kasdorf; Matthias Marczynski; Michael T Cross; Lydia J Finney; Maria-Belen Trujillo Torralbo; Maria Calderazzo; Jie Zhu; Julia Aniscenko; Thomas B Clarke; Philip L Molyneaux; Nathan W Bartlett; Miriam F Moffatt; William O Cookson; Jadwiga Wedzicha; Christopher M Evans; Oliver Lieleg; Patrick Mallia; Sebastian L Johnston
Title: MUC5AC drives COPD exacerbation severity through amplification of virus-induced airway inflammation Document date: 2019_7_22
ID: gg2ctmn7_4
Snippet: Here, using human studies in combination with functional experiments in mouse models, we identify a central and unforeseen role for MUC5AC in amplifying virus-induced airway inflammation and driving subsequent exacerbation severity in COPD. We identify a mechanism for augmentation of virus-induced inflammation by MUC5AC through release of extracellular adenosine triphosphate (ATP) and show that therapeutic suppression of virusinduced MUC5AC relea.....
Document: Here, using human studies in combination with functional experiments in mouse models, we identify a central and unforeseen role for MUC5AC in amplifying virus-induced airway inflammation and driving subsequent exacerbation severity in COPD. We identify a mechanism for augmentation of virus-induced inflammation by MUC5AC through release of extracellular adenosine triphosphate (ATP) and show that therapeutic suppression of virusinduced MUC5AC release using an epidermal growth factor receptor (EGFR) inhibitor ameliorates exaggerated pro-inflammatory responses in a mouse COPD exacerbation model. Our studies are the first to implicate MUC5AC as a key functional driver of COPD author/funder. All rights reserved. No reuse allowed without permission.
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