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J Appl Physiol (February 13, 2004). doi:10.1152/japplphysiol.00960.2003
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Submitted on September 5, 2003
Accepted on February 9, 2004

DIFFERENTIAL EFFECTS OF OZONE ON AIRWAY AND TISSUE MECHANICS IN OBESE MICE

Yadira M Rivera-Sanchez1, Richard A Johnston1, Igor N Schwartzman1, Joseph Valone1, Eric S Silverman1, Jeffrey J Fredberg1, and Stephanie A Shore1*

1 Physiology Program, Harvard School of Public Health, Boston, MA, USA

* To whom correspondence should be addressed. E-mail: sshore{at}hsph.harvard.edu.

Obesity is an important risk factor for asthma. We recently reported increased ozone (O3)-induced hyperresponsiveness to methacholine in obese mice. The purpose of this study was to determine whether this increased hyperresponsiveness is the result of changes in the airways, the lung tissue or both. To that end, we examined the effect of O3 (2 ppm for 3 h) on methacholine-induced changes in lung mechanics using a forced oscillation technique in wildtype C57BL/6J mice and mice obese because of a genetic deficiency in leptin (ob/ob mice). In ob/ob mice O3 increased baseline values for all the parameters measured in the study: airway resistance (Raw), lung tissue resistance (Rtis), lung tissue damping (G) and elastance (H), and lung hysteresivity ({eta}). In contrast, no effect of O3 on baseline mechanics was observed in wildtype mice. O3 exposure significantly increased Raw, Rtis, RL, G, H, and {eta} responses to methacholine in both groups of mice. For G, Rtis, and RL there was a significant effect of obesity. Our results demonstrate that both airways and lung tissue contribute to the hyperresponsiveness that occurs following O3 exposure in wildtype mice. Our results also demonstrate that changes in the lung tissue rather than the airways account for the amplification of O3-induced hyperresponsiveness observed in obese mice.




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