- Title
- Bromodomain and extra terminal (BET) inhibitor suppresses macrophage-driven steroid-resistant exacerbations of airway hyper-responsiveness and inflammation
- Creator
- Nguyen, Thi Hiep; Maltby, Steven; Eyers, Fiona; Foster, Paul S.; Yang, Ming
- Relation
- NHMRC.1060660 http://purl.org/au-research/grants/nhmrc/1060660
- Relation
- PLoS One Vol. 11, Issue 9, no. e0163392
- Publisher Link
- http://dx.doi.org/10.1371/journal.pone.0163392
- Publisher
- Public Library of Science (PLoS)
- Resource Type
- journal article
- Date
- 2016
- Description
- Exacerbations of asthma are linked to significant decline in lung function and are often poorly controlled by corticosteroid treatment. Clinical investigations indicate that viral and bacterial infections play crucial roles in the onset of steroid-resistant inflammation and airways hyperresponsiveness (AHR) that are hallmark features of exacerbations.We have previously shown that interferon γ (IFNγ) and lipopolysaccharide (LPS) cooperatively activate pulmonary macrophages and induce steroid-resistant airway inflammation and AHR in mouse models. Furthermore, we have established a mouse model of respiratory syncytial virus (RSV)-induced exacerbation of asthma, which exhibits macrophage-dependent, steroid- resistant lung disease. Emerging evidence has demonstrated a key role for bromoand extra-terminal (BET) proteins in the regulation of inflammatory gene expression in macrophages. We hypothesised that BET proteins may be involved in the regulation of AHR and airway inflammation in our steroid-resistant exacerbation models.
- Subject
- macrophages; inflammation; mouse models; asthma; inflammatory diseases; neutrophils; cytokines; eosinophils
- Identifier
- http://hdl.handle.net/1959.13/1348044
- Identifier
- uon:30136
- Identifier
- ISSN:1932-6203
- Rights
- © 2016 Nguyen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
- Language
- eng
- Full Text
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