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

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The allergic mouse model of asthma: normal smooth muscle in an abnormal lung? / Wagers, S; Lundblad, Lennart; Ekman, Mari; Irvin, CG; Bates, JHT.

In: Journal of Applied Physiology, Vol. 96, No. 6, 2004, p. 2019-2027.

Research output: Contribution to journalArticle

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Wagers, S ; Lundblad, Lennart ; Ekman, Mari ; Irvin, CG ; Bates, JHT. / The allergic mouse model of asthma: normal smooth muscle in an abnormal lung?. In: Journal of Applied Physiology. 2004 ; Vol. 96, No. 6. pp. 2019-2027.

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TY - JOUR

T1 - The allergic mouse model of asthma: normal smooth muscle in an abnormal lung?

AU - Wagers, S

AU - Lundblad, Lennart

AU - Ekman, Mari

AU - Irvin, CG

AU - Bates, JHT

PY - 2004

Y1 - 2004

N2 - 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.

AB - 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.

KW - mucosal thickening

KW - elastance

KW - resistance

KW - inflammation

KW - lung impedance

U2 - 10.1152/japplphysiol.00924.2003

DO - 10.1152/japplphysiol.00924.2003

M3 - Article

VL - 96

SP - 2019

EP - 2027

JO - Journal of Applied Physiology

T2 - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 1522-1601

IS - 6

ER -