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Published ahead of print on November 9, 2006, doi:10.1164/rccm.200509-1493OC

Am. J. Respir. Crit. Care Med., Volume 175, Number 2, January 2007, 126-135

A more recent version of this article appeared on January 15, 2007
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Submitted on September 23, 2005
Accepted on November 3, 2006

Spontaneous Airway Hyperresponsiveness in Estrogen Receptor-{alpha} Deficient Mice

Michelle A Carey1, Jeffrey W Card1, J. Alyce Bradbury1, Michael P Moorman1, Najwa Haykal-Coates2, Stephen H Gavett2, Joan P Graves1, Vickie R Walker1, Gordon P Flake1, James W Voltz1, Daling Zhu3, Elizabeth R Jacobs3, Azzeddine Dakhama4, Gary L Larsen4, Joan E Loader4, Erwin W Gelfand4, Dori R Germolec1, Kenneth S Korach1, and Darryl C Zeldin1*

1 National Institute of Environmental Health Sciences, Division of Intramural Research, National Institutes of Health, Research Triangle Park, NC, USA, 2 National Health and Environmental Effects Research Laboratory, Experimental Toxicology Division, U.S. Environmental Protection Agency, Research Triangle Park, NC, USA, 3 Cardiovascular Research Center, Departments of Medicine and Physiology, Medical College of Wisconsin, Milwaukee, WI, USA, 4 Division of Cell Biology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO, USA

* To whom correspondence should be addressed. E-mail: zeldin{at}niehs.nih.gov.

Rationale: Airway hyperresponsiveness is a critical feature of asthma. Substantial epidemiologic evidence supports a role for female sex hormones in modulating lung function and airway hyperresponsiveness in humans. Objectives: To examine the role of estrogen receptors in modulating lung function and airway responsiveness using estrogen receptor deficient mice. Methods: Lung function was assessed by a combination of whole body barometric plethysmography, invasive measurement of airway resistance and isometric force measurements in isolated bronchial rings. M2 muscarinic receptor expression was assessed by western blotting and function was assessed by electrical field stimulation of tracheas in the presence/absence of gallamine. Allergic airway disease was examined following ovalbumin sensitization and exposure. Measurements and main results: Estrogen receptor-{alpha} knockout mice exhibit a variety of lung function abnormalities and have enhanced airway responsiveness to inhaled methacholine and serotonin under basal conditions. This is associated with reduced M2 muscarinic receptor expression and function in the lungs. Absence of estrogen receptor-{alpha} also leads to increased airway responsiveness without increased inflammation following allergen sensitization and challenge. Conclusions: These data suggest that estrogen receptor-{alpha} is a critical regulator of airway hyperresponsiveness in mice.
Key words: lung function, asthma, hyperreactivity, M2 muscarinic receptor, estrogen receptor




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