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_64
Snippet: Female mice (age 6-8 weeks) purchased from Charles River Laboratories on a C57BL/6 background were used for all wild-type animal studies. Muc5ac-/-mice were generated on a C57BL/6 background at the University of Colorado, as previously described 11 For evaluation of EGFR inhibitor in a COPD exacerbation model, as previously reported 24 , mice were treated intranasally under light isoflurane anaesthesia with 1.2 units of porcine pancreatic elastas.....
Document: Female mice (age 6-8 weeks) purchased from Charles River Laboratories on a C57BL/6 background were used for all wild-type animal studies. Muc5ac-/-mice were generated on a C57BL/6 background at the University of Colorado, as previously described 11 For evaluation of EGFR inhibitor in a COPD exacerbation model, as previously reported 24 , mice were treated intranasally under light isoflurane anaesthesia with 1.2 units of porcine pancreatic elastase (Merck, UK) to induce COPD-like changes. Ten days following elastase administration, as previously described 46 , mice were treated intraperitoneally with 50mg/kg of the EGFR inhibitor AG1478, 16 hours prior to intranasal infection with 50μL RV-A1 (2.5 x 10 6 TCID 50 ) or UV-inactivated RV-A1 control.
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