Murine models of COPD

Murine models of COPD

Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation, that is not fully reversible, and that is associated with an abnormal inflammatory response of the airways and lungs to noxious particles and gases. The airflow limitation is caused by increased resistance of the sm...

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Bibliographic Details
Published in:Pulmonary pharmacology & therapeutics Vol. 19; no. 3; pp. 155 - 165
Main Authors: Brusselle, G.G., Bracke, K.R., Maes, T., D'hulst, A.I., Moerloose, K.B., Joos, G.F., Pauwels, R.A.
Format: Journal Article
Language:English
Published: England Elsevier Ltd 01-01-2006
Subjects:
Animals
Apoptosis
Cigarette smoke
COPD
Disease Models, Animal
Emphysema
Humans
Inflammation
Mice
Mice, Transgenic
Murine
Pulmonary Disease, Chronic Obstructive - genetics
Pulmonary Disease, Chronic Obstructive - physiopathology
VEGF
MMP(s)
Inflammation
BAL
IL (e.g. IL-1, IL-6, IL-8)
LPS
CS
NF-κB
IFN-γ
TEAC
TNF-α
RT-PCR
VEGFR-2
ROS
TGF-β
FEV1
TLR (e.g. TLR-4)
LBP
Emphysema
Murine
Cigarette smoke
COPD
Apoptosis
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Description
Summary:Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation, that is not fully reversible, and that is associated with an abnormal inflammatory response of the airways and lungs to noxious particles and gases. The airflow limitation is caused by increased resistance of the small conducting airways and by decreased elastic recoil forces of the lung due to emphysematous destruction of the lung parenchyma. In vivo animal models can help to unravel the molecular and cellular mechanisms underlying the pathogenesis of COPD. Mice represent the most favored animal species with regard to the study of (both innate and adaptive) immune mechanisms, since they offer the opportunity to manipulate gene expression. Several experimental approaches are applied in order to mimic the different traits of COPD in these murine models. Firstly, the tracheal instillation of tissue-degrading enzymes induces emphysema-like lesions in the lung parenchyma, adding further proof to the protease-antiprotease imbalance hypothesis. Secondly, the inhalation of noxious stimuli, including tobacco smoke, sulfur dioxide, nitrogen dioxide, or oxidants such as ozone, may also lead to COPD-like lesions in mice, depending on concentration, duration of exposure and strainspecific genetic susceptibility. Thirdly, in transgenic mice, a specific gene is either overexpressed (non-specific or organ-specific) or selectively depleted (constitutively or conditionally). The study of these transgenic mice, either per se or in combination with the above mentioned experimental approaches (e.g. the inhalation of tobacco smoke), can offer valuable information on both the physiological function of the gene of interest as well as the pathophysiological mechanisms of diseases with complex traits such as COPD.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
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ObjectType-Review-1
ISSN:1094-5539
1522-9629
DOI:10.1016/j.pupt.2005.06.001