The allergic mouse model of asthma: normal smooth muscle in an abnormal lung?

Research output: Contribution to journalArticle

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.

Details

Authors
  • S Wagers
  • Lennart Lundblad
  • Mari Ekman
  • CG Irvin
  • JHT Bates
Organisations
Research areas and keywords

Subject classification (UKÄ) – MANDATORY

  • Physiology

Keywords

  • mucosal thickening, elastance, resistance, inflammation, lung impedance
Original languageEnglish
Pages (from-to)2019-2027
JournalJournal of Applied Physiology
Volume96
Issue number6
StatePublished - 2004
Peer-reviewedYes