Abstract
Although asthma is characterized as an inflammatory disease, recent reports highlight the importance of pulmonary physiology outcome measures to the clinical assessment of asthma control and risk of asthma exacerbation. Murine models of allergic inflammatory airway disease have been widely used to gain mechanistic insight into the pathogenesis of asthma; however, several aspects of murine models could benefit from improvement. This review focuses on aligning lung mechanics measures made in mice with those made in humans, with an eye toward improving the translational utility of these measures. A brief description of techniques available to measure murine lung mechanics is provided along with a methodological consideration of their utilization. How murine lung mechanics outcome measures relate to pulmonary physiology measures conducted in humans is discussed and we recommend that, like human studies, outcome measures be standardized for murine models of asthma.
Highlights
ASSESSING OUTCOME MEASURES IN MURINE MODELS OF ASTHMASYMPTOMS AND INFLAMMATION The murine correlate to asthmatic signs and symptoms is lacking
SUMMARY AND CONCLUSION The American Thoracic Society (ATS) recently assembled a task force charged with defining asthma control and determining the clinical outcome measures important for its assessment
The ensuing report clearly advocates that lung function and airway hyperresponsiveness (AHR) be the principal outcome measures utilized in both clinical practice and clinical trials to guide treatment and evaluation of new therapies, respectively
Summary
SYMPTOMS AND INFLAMMATION The murine correlate to asthmatic signs and symptoms is lacking. In a remarkable foreshadowing of the explosion of murine models of asthma, Martin et al (1988) alluded to the attractiveness of murine models in immunology and genetics coupled with an acute need for robust measures of pulmonary mechanics and airway responsiveness They successfully scaled-down standard plethysmographic techniques for measuring RL (and its reciprocal conductance) and dynamic pulmonary compliance (Cdyn) (and its reciprocal elastance) in larger animal models (Mead, 1961) to accurately assess these variables in the mouse during intravenous challenge with a range of bronchoconstrictor and BD agents.
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