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_25
Snippet: We next sought to further understand the functional importance of MUC5AC during RV infection using mouse models in which cause and effect relationships can readily be assessed. Mice with gene-targeted deletion of Muc5ac (Muc5ac-/-) (Fig.3a) had attenuated cellular airway inflammation (BAL total cell counts and neutrophil numbers; Fig.3b ) and reduced concentrations of the neutrophil chemokines CXCL1/KC and CXCL2/MIP-2 ( Fig. 3c ) following RV i.....
Document: We next sought to further understand the functional importance of MUC5AC during RV infection using mouse models in which cause and effect relationships can readily be assessed. Mice with gene-targeted deletion of Muc5ac (Muc5ac-/-) (Fig.3a) had attenuated cellular airway inflammation (BAL total cell counts and neutrophil numbers; Fig.3b ) and reduced concentrations of the neutrophil chemokines CXCL1/KC and CXCL2/MIP-2 ( Fig. 3c ) following RV infection compared to wild-type controls. BAL concentrations of the proinflammatory cytokines IL-1b, IL-6 and TNF were also reduced in RV-infected Muc5ac-/mice compared to wild-type controls (Fig. 3d) . The pro-inflammatory effects of MUC5AC
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