About: MUC5AC drives COPD exacerbation severity through amplification of virus-induced airway inflammation

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About: MUC5AC drives COPD exacerbation severity through amplification of virus-induced airway inflammation Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	MUC5AC drives COPD exacerbation severity through amplification of virus-induced airway inflammation
Creator	Zhu, Jie Calderazzo, Maria Footitt, Joseph Mallia, Patrick Singanayagam, Aran Bartlett, Nathan Johnston, Sebastian Aniscenko, Julia Clarke, Thomas Cookson, William Cross, Michael Evans, Christopher Finney, Lydia Kasdorf, Benjamin Lieleg, Oliver Marczynski, Matthias Moffatt, Miriam Molyneaux, Philip Trujillo, Maria-Belen Wedzicha, Jadwiga
Source	BioRxiv; MedRxiv
abstract	The respiratory tract surface is protected from inhaled pathogens by a secreted layer of mucus that is rich in mucin glycoproteins. Disrupted mucus production is a cardinal feature of chronic respiratory diseases but how this alteration affect interactions between mucins and pathogens is complex and poorly understood. Here, we identify a central and unexpected role for the major airway mucin MUC5AC in pathogenesis of virus-induced exacerbations of chronic obstructive pulmonary disease (COPD). Virus induction of MUC5AC is augmented in COPD compared to healthy subjects, is enhanced in frequent exacerbators and correlates with inflammation, symptom severity and secondary bacterial infection during exacerbation. MUC5AC is functionally related to inflammation as MUC5AC-deficient (Muc5ac-/-) mice had attenuated rhinovirus-induced airway inflammation whilst exogenous MUC5AC glycoprotein administration augmented virus-induced inflammatory responses and bacterial load. Mechanistically, MUC5AC-augmentation of rhinovirus-induced inflammation occurred through release of extracellular adenosine triphosphate (ATP). Therapeutic suppression of virus-induced MUC5AC release using an epidermal growth factor receptor (EGFR) inhibitor ameliorated exaggerated pro-inflammatory responses in a mouse COPD exacerbation model. Collectively, these studies demonstrate previously unrecognised pro-inflammatory effects of MUC5AC during infection and thus highlight a key unforeseen role in driving COPD exacerbation severity.
has issue date	2019-07-22(xsd:dateTime)
bibo:doi	10.1101/706804
has license	medrxiv
sha1sum (hex)	9c32d461dc9d4737756a990cf13bae1a03e078a9
schema:url	https://doi.org/10.1101/706804
resource representing a document's title	MUC5AC drives COPD exacerbation severity through amplification of virus-induced airway inflammation
schema:publication	bioRxiv
resource representing a document's body	covid:9c32d461dc9d4737756a990cf13bae1a03e078a9#body_text
is schema:about of	named entity 'SEVERITY' named entity 'MUC5AC' named entity 'MUC5AC' named entity 'functionally' named entity 'extracellular' named entity 'VIRUS' named entity 'DRIVES' named entity 'COPD EXACERBATION' named entity 'IDENTIFY' named entity 'MODEL' named entity 'AUGMENTATION' named entity 'MICE' named entity 'INHIBITOR' named entity 'PREVIOUSLY' named entity 'MUC5AC' named entity 'OCCURRED' named entity 'LAYER' named entity 'ROLE' named entity 'THERAPEUTIC' named entity 'AIRWAY' named entity 'EPIDERMAL GROWTH FACTOR RECEPTOR' named entity 'SURFACE' named entity 'COMPLEX' named entity 'MUCINS' named entity 'MUCUS' named entity 'INDUCED' named entity 'SECRETED' named entity 'AIRWAY INFLAMMATION' named entity 'PATHOGENESIS' named entity 'INHALED' named entity 'EXOGENOUS' named entity 'INTERACTIONS' named entity 'MUCUS PRODUCTION' named entity 'AIRWAY INFLAMMATION' named entity 'AMPLIFICATION' named entity 'INDUCED' named entity 'UNEXPECTED' named entity 'CENTRAL' named entity 'THESE' named entity 'SYMPTOM SEVERITY' named entity 'GLYCOPROTEIN' named entity 'MUC5AC' named entity 'VIRUS' named entity 'CARDINAL' named entity 'INFECTION' named entity 'IS A' named entity 'INFLAMMATION' named entity 'DISRUPTED' named entity 'PATHOGENS' named entity 'GLYCOPROTEINS' named entity 'STUDIES' named entity 'POORLY' named entity 'INDUCTION' named entity 'HEALTHY SUBJECTS' named entity 'EXTRACELLULAR' named entity 'RICH' named entity 'EXACERBATION' named entity 'RESPIRATORY TRACT' named entity 'CHRONIC OBSTRUCTIVE PULMONARY DISEASE' named entity 'PRO-INFLAMMATORY RESPONSES' named entity 'CHRONIC' named entity 'RESPIRATORY DISEASES' named entity 'SUPPRESSION' named entity 'UNDERSTOOD' named entity 'ATTENUATED'

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