| Literature DB >> 31352362 |
Florence Chau-Etchepare1, Joshua L Hoerger2, Brooks T Kuhn1, Amir A Zeki1,3, Angela Haczku1,3, Samuel Louie1, Nicholas J Kenyon1,3, Cristina E Davis4, Michael Schivo1,3.
Abstract
Asthma is a complex inflammatory disease with many triggers. The best understood asthma inflammatory pathways involve signals characterized by peripheral eosinophilia and elevated immunoglobulin E levels (called T2-high or allergic asthma), though other asthma phenotypes exist (eg, T2-low or non-allergic asthma, eosinophilic or neutrophilic-predominant). Common triggers that lead to poor asthma control and exacerbations include respiratory viruses, aeroallergens, house dust, molds, and other organic and inorganic substances. Increasingly recognized non-allergen triggers include tobacco smoke, small particulate matter (eg, PM2.5), and volatile organic compounds. The interaction between respiratory viruses and non-allergen asthma triggers is not well understood, though it is likely a connection exists which may lead to asthma development and/or exacerbations. In this paper we describe common respiratory viruses and non-allergen triggers associated with asthma. In addition, we aim to show the possible interactions, and potential synergy, between viruses and non-allergen triggers. Finally, we introduce a new clinical approach that collects exhaled breath condensates to identify metabolomics associated with viruses and non-allergen triggers that may promote the early management of asthma symptoms. © American Federation for Medical Research 2019. No commercial re-use. See rights and permissions. Published by BMJ.Entities:
Keywords: asthma; tobacco
Year: 2019 PMID: 31352362 DOI: 10.1136/jim-2019-001000
Source DB: PubMed Journal: J Investig Med ISSN: 1081-5589 Impact factor: 2.895