Selected article for: "cystic fibrosis and danger signal"
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_51
    Snippet: We identified a mechanism for amplification of rhinovirus-induced airway inflammation by MUC5AC through release of ATP, a danger signal that is released during infection and contributes to nucleotide receptor-dependent inflammatory responses 32 . This mechanism was suggested in a previous study that indicated that administration of sterile supernatants of mucopurulent material from subjects with cystic fibrosis can induce ATP release by human bro.....
    Document: We identified a mechanism for amplification of rhinovirus-induced airway inflammation by MUC5AC through release of ATP, a danger signal that is released during infection and contributes to nucleotide receptor-dependent inflammatory responses 32 . This mechanism was suggested in a previous study that indicated that administration of sterile supernatants of mucopurulent material from subjects with cystic fibrosis can induce ATP release by human bronchial epithelial cells in vitro 20 . The role of ATP as a potential driver of airway inflammation in stable asthma and COPD is well recognised 33,34 . Our findings, in models of infection, that neutralisation of pulmonary ATP levels abrogates MUC5AC enhancement of author/funder. All rights reserved. No reuse allowed without permission.

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