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Am J Physiol Regul Integr Comp Physiol (July 7, 2005). doi:10.1152/ajpregu.00306.2005
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Submitted on April 29, 2005
Accepted on July 7, 2005

AUGMENTED RESPONSES TO OZONE IN OBESE CARBOXYPEPTIDASE E-DEFICIENT MICE

Richard A Johnston1*, Todd A Theman1, and Stephanie A Shore1

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

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

We reported previously that mice obese as a result of leptin deficiency (ob/ob) have enhanced ozone (O3)-induced airway hyperresponsiveness (AHR) and inflammation compared to wildtype (C57BL/6) controls. To determine whether this increased response to O3 was independent of the modality of obesity, we examined O3-induced AHR and inflammation in Cpefat mice. These mice are obese as a consequence of a mutation in the gene encoding carboxypeptidase E (Cpe), an enzyme important in processing prohormones and proneuropeptides involved in satiety and energy expenditure. Airway responsiveness to intravenous methacholine, measured by forced oscillation, was increased in Cpefat versus wildtype mice after air exposure. In addition, compared to air exposure, airway responsiveness was increased 24 h after O3 exposure (2 ppm for 3 h) in Cpefat but not in wildtype mice. Compared to air-exposed controls, O3 exposure increased bronchoalveolar lavage fluid (BALF) protein, IL-6, KC, MIP-2, MCP-1, and soluble TNF receptors (sTNFR1 and sTNFR2) as well as BALF neutrophils. With the exception of sTNFR1 and sTNFR2, all of these outcome indicators were greater in Cpefat versus wildtype mice. Serum sTNFR1, sTNFR2, MCP-1, leptin, and blood leukocytes were elevated in Cpefat compared to wildtype mice even in the absence of O3 exposure, similar to the chronic systemic inflammation observed in human obesity. These results indicate that increased O3-induced AHR and inflammation are consistent features of obese mice, regardless of the modality of obesity. These results also suggest that chronic systemic inflammation may enhance airway responses to O3 in obese mice.




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