Abstract：
BACKGROUND:Our recently developed murine asthma model is capable of inducing airway-specific chronic inflammatory changes and remodeling, features of human asthma commonly missing in conventional animal models. OBJECTIVES:To validate this model by site-specific physiological evaluation of hyperresponsiveness. METHODS:Non-sensitized and sensitized mice received either short-term uncontrolled or long-term controlled low-level exposures to aerosolized ovalbumin (OVA). Respiratory impedance (Zrs) was measured in response to increasing doses of methacholine (Mch). The constant-phase model was fitted to Zrs spectra to determine the specific site of hyperresponsiveness. RESULTS:Sensitized acutely exposed mice had significantly increased tissue damping (G), tissue elastance (H) and hysteresivity (eta) in response to Mch, but no significant increase in airway resistance (Raw), indicating tissue-specific hyperresponsiveness. In contrast, sensitized chronically exposed mice had significantly elevated Raw at all concentrations of Mch but no increases in G, H or eta indicating airway-specific hyperresponsiveness. CONCLUSIONS:Chronic inhalational exposure of sensitized mice to low-mass concentrations of OVA induces airway-specific hyperresponsiveness.
journal_name
Respir Physiol Neurobioljournal_title
Respiratory physiology & neurobiologyauthors
Collins RA,Sly PD,Turner DJ,Herbert C,Kumar RKdoi
10.1016/j.resp.2003.09.003keywords:
subject
Has Abstractpub_date
2003-12-16 00:00:00pages
51-61issue
1eissn
1569-9048issn
1878-1519pii
S1569904803002283journal_volume
139pub_type
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