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Characterisation of a Mouse Model of Cigarette Smoke Extract-Induced Lung Inflammation | OMICS International | Abstract
ISSN: 2161-105X

Journal of Pulmonary & Respiratory Medicine
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Research Article

Characterisation of a Mouse Model of Cigarette Smoke Extract-Induced Lung Inflammation

David J. Lamb*, Nicole Parker, Kristina Ulrich, Roddy Walsh, Mike Yeadon and Steven M. Evans

Internal Medicine Research Unit, Pfizer Global Research & Development, Ramsgate Road, Sandwich, Kent, CT13 9NJ, UK

*Corresponding Author:
David J Lamb
Department Respiratory Disease Research
Boehringer Ingelheim Pharma GmbH & Co. KG
Birkendorfer Straße 65, 88397 Biberach an der Riß, Germany
Tel: 49735154141403
E-mail: [email protected]

Received date:January 04, 2012; Accepted date: June 22, 2012; Published date:June 24, 2012

Citation: Lamb DJ, Parker N, Ulrich K, Walsh R, Yeadon M, et al. (2012) Characterisation of a Mouse Model of Cigarette Smoke Extract-Induced Lung Inflammation. J Pulmon Resp Med 2:125. doi:10.4172/2161-105X.1000125

Copyright: © 2012 Lamb DJ, 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.

Abstract

Aim: The aim of this study was to develop a lung-targeted, mouse model of cigarette smoke-induced inflammation that can be used to study the pathophysiological changes that occur in the lungs of human smokers and patients with chronic obstructive pulmonary disease (COPD).

Materials & methods: Cigarette smoke extract (CSE) was prepared freshly daily. Intranasal administration into female mice was performed once daily for up to 3 weeks.

Results: CSE significantly increased airway macrophages after 3 and 4 days of dosing, and then declined over the subsequent 2 weeks. However, airway neutrophils were elevated after a single dose of CSE, and at all subsequent time points. Muc5AC was significantly increased in the Bronchoalveolar lavage (BAL) of CSE-treated animals compared to control mice (P<0.05), but TNF-α concentrations decreased in a dose-dependent manner. In animals challenged with CSE for 4 consecutive days, a PDE4 inhibitor (Roflumilast; 10 mg/kg BID) significantly inhibited both macrophages (P<0.01) and neutrophils (P<0.001), a steroid (prednisolone; 10 mg/kg BID) had no effect on either macrophages or neutrophils and an oral p38 inhibitor (PHA-818637; 10 mg/kg BID) inhibited macrophages (P<0.05), but not neutrophils. CSE inhibited lipopolysaccharide-induced airway neutrophilia.

Conclusion: This model reflects many aspects of human COPD including pulmonary leucocytes, mucin, TNF-α and response to clinical therapeutic agents and may be useful in assessing the efficacy of potential therapies

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