Toll-Like Receptor-9 Agonist Inhibits Airway Inflammation, Remodeling and Hyperreactivity in Mice Exposed to Chronic Environmental Tobacco Smoke and Allergen
- Authors
- Song, Dae Jin; Min, Myung Goo; Miller, Marina; Cho, Jae Youn; Yum, Hye Yung; Broide, David H.
- Issue Date
- 2010
- Publisher
- KARGER
- Keywords
- Toll-like receptor-9; Airway hyperreactivity; Airway inflammation; Airway remodeling; Eosinophils
- Citation
- INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY, v.151, no.4, pp.285 - 296
- Indexed
- SCIE
SCOPUS
- Journal Title
- INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY
- Volume
- 151
- Number
- 4
- Start Page
- 285
- End Page
- 296
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/118545
- DOI
- 10.1159/000250437
- ISSN
- 1018-2438
- Abstract
- Background: As passive environmental tobacco smoke (ETS) exposure in nonsmokers can increase both asthma symptoms and the frequency of asthma exacerbations, we utilized a mouse model, in which ovalbumin (OVA) + ETS induce significantly increased levels of eosinophilic airway inflammation and remodeling compared to either stimulus alone, to determine whether a Toll-like receptor-9 (TLR-9) agonist could reduce levels of airway inflammation, airway remodeling and airway hyperreactivity (AHR). Methods: Mice treated with or without a TLR-9 agonist were sensitized to OVA and challenged with OVA + ETS for 1 month. AHR to methacholine was assessed in intubated and ventilated mice. Lung Th2 cytokines and TGF-beta(1) were measured by ELISA. Lungs were processed for histology and immunohistology to quantify eosinophils, mucus, peribronchial fibrosis and smooth muscle changes using image analysis. Results: Administration of a TLR-9 agonist to mice coexposed to chronic ETS and chronic OVA allergen significantly reduced levels of eosinophilic airway inflammation, mucus production, peribronchial fibrosis, the thickness of the peribronchial smooth muscle lay-er, and AHR. The reduced airway remodeling in mice treated with the TLR-9 agonist was associated with significantly reduced numbers of peribronchial MBP+ and peribronchial TGF-beta(1) + cells, and with significantly reduced levels of lung Th2 cytokines [interleukin-5 and interleukin-13] and TGF-beta(1). Conclusion: These studies demonstrate that TLR-9-based therapies inhibit airway inflammation, remodeling and AHR in mice coexposed to ETS and allergen who exhibit enhanced airway inflammation and remodeling. Copyright (C) 2009 S. Karger AG, Basel
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