Publication:
Airway remodelling in asthma and novel therapy

dc.contributor.authorWiparat Manuyakornen_US
dc.contributor.authorPeter H. Howarthen_US
dc.contributor.authorStephen T. Holgateen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherSouthampton General Hospitalen_US
dc.date.accessioned2018-10-19T05:05:18Z
dc.date.available2018-10-19T05:05:18Z
dc.date.issued2013-03-01en_US
dc.description.abstractAsthma is an airway inflammatory disease with functional and structural changes, leading to bronchial hyperresponsiveness (BHR) and airflow obstruction. Airway structural changes or airway remodelling consist of epithelial injury, goblet cell hyperplasia, subepithelial layer thickening, airway smooth muscle hyperplasia and angiogenesis. These changes were previously considered as a consequence of chronic airway inflammation. However, several studies have demonstrated that inflammation and remodelling can occur as separate but parallel aspects of the asthmatic process. As such there is increasing evidence for the role of mechanocompressive forces within the asthmatic airway contributing to airway structural changes. Furthermore, it is unclear what is the best treatment to modify remodelling and which component to target. There is also a need to identify asthma phenotype that might specifically respond to novel therapies such as anti-IL5, anti-IL13 and tyrosine kinase inhibitors.en_US
dc.identifier.citationAsian Pacific Journal of Allergy and Immunology. Vol.31, No.1 (2013), 3-10en_US
dc.identifier.issn22288694en_US
dc.identifier.issn0125877Xen_US
dc.identifier.other2-s2.0-84873556164en_US
dc.identifier.urihttps://repository.li.mahidol.ac.th/handle/20.500.14594/31957
dc.rightsMahidol Universityen_US
dc.rights.holderSCOPUSen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84873556164&origin=inwarden_US
dc.subjectImmunology and Microbiologyen_US
dc.subjectMedicineen_US
dc.titleAirway remodelling in asthma and novel therapyen_US
dc.typeReviewen_US
dspace.entity.typePublication
mu.datasource.scopushttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84873556164&origin=inwarden_US

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