The allergic mouse model of asthma: normal smooth muscle in an abnormal lung?
(2004) In Journal of Applied Physiology 96(6). p.2019-2027- Abstract
- Mice with allergically inflamed airways are widely used as animal models of asthma, but their relevance for human asthma is not understood. We, therefore, examined the time course of changes in respiratory input impedance during induced bronchoconstriction in BALB/c mice sensitized and challenged with ovalbumin. Our results indicate that bronchoconstriction in mice is accompanied by complete closure of substantial regions of the lung and that closure increases markedly when the lungs are allergically inflamed. With the aid of an anatomically accurate computational model of the mouse lung, we show that the hyperresponsiveness of mice with allergically inflamed airways can be explained entirely by a thickening of the airway mucosa and an... (More)
- Mice with allergically inflamed airways are widely used as animal models of asthma, but their relevance for human asthma is not understood. We, therefore, examined the time course of changes in respiratory input impedance during induced bronchoconstriction in BALB/c mice sensitized and challenged with ovalbumin. Our results indicate that bronchoconstriction in mice is accompanied by complete closure of substantial regions of the lung and that closure increases markedly when the lungs are allergically inflamed. With the aid of an anatomically accurate computational model of the mouse lung, we show that the hyperresponsiveness of mice with allergically inflamed airways can be explained entirely by a thickening of the airway mucosa and an increased propensity of the airways to close, without the involvement of any increase in the degree of airway smooth muscle shortening. This has implications for the pathophysiology of asthma and suggests that at least some types of asthma may benefit from therapies aimed at manipulating surface tension at the air-liquid interface in the lungs. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/279406
- author
- Wagers, S ; Lundblad, Lennart LU ; Ekman, Mari LU ; Irvin, CG and Bates, JHT
- organization
- publishing date
- 2004
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- mucosal thickening, elastance, resistance, inflammation, lung impedance
- in
- Journal of Applied Physiology
- volume
- 96
- issue
- 6
- pages
- 2019 - 2027
- publisher
- American Physiological Society
- external identifiers
-
- wos:000221296600002
- pmid:14660507
- scopus:2442715233
- pmid:14660507
- ISSN
- 1522-1601
- DOI
- 10.1152/japplphysiol.00924.2003
- language
- English
- LU publication?
- yes
- id
- fce9b231-8e81-4b98-954d-535eb8fad0fa (old id 279406)
- date added to LUP
- 2016-04-01 12:37:37
- date last changed
- 2025-04-04 14:12:25
@article{fce9b231-8e81-4b98-954d-535eb8fad0fa,
abstract = {{Mice with allergically inflamed airways are widely used as animal models of asthma, but their relevance for human asthma is not understood. We, therefore, examined the time course of changes in respiratory input impedance during induced bronchoconstriction in BALB/c mice sensitized and challenged with ovalbumin. Our results indicate that bronchoconstriction in mice is accompanied by complete closure of substantial regions of the lung and that closure increases markedly when the lungs are allergically inflamed. With the aid of an anatomically accurate computational model of the mouse lung, we show that the hyperresponsiveness of mice with allergically inflamed airways can be explained entirely by a thickening of the airway mucosa and an increased propensity of the airways to close, without the involvement of any increase in the degree of airway smooth muscle shortening. This has implications for the pathophysiology of asthma and suggests that at least some types of asthma may benefit from therapies aimed at manipulating surface tension at the air-liquid interface in the lungs.}},
author = {{Wagers, S and Lundblad, Lennart and Ekman, Mari and Irvin, CG and Bates, JHT}},
issn = {{1522-1601}},
keywords = {{mucosal thickening; elastance; resistance; inflammation; lung impedance}},
language = {{eng}},
number = {{6}},
pages = {{2019--2027}},
publisher = {{American Physiological Society}},
series = {{Journal of Applied Physiology}},
title = {{The allergic mouse model of asthma: normal smooth muscle in an abnormal lung?}},
url = {{http://dx.doi.org/10.1152/japplphysiol.00924.2003}},
doi = {{10.1152/japplphysiol.00924.2003}},
volume = {{96}},
year = {{2004}},
}