https://scholars.lib.ntu.edu.tw/handle/123456789/524940
標題: | Diet-induced obesity causes innate airway hyperresponsiveness to methacholine and enhances ozone-induced pulmonary inflammation | 作者: | Johnston R.A. Theman T.A. FRANK LEIGH LU Terry R.D. Williams E.S. Shore S.A. |
關鍵字: | Bronchoalveolar lavage fluid; Chemokine; Leptin; Lung elastance; Resistance | 公開日期: | 2008 | 卷: | 104 | 期: | 6 | 起(迄)頁: | 1727-1735 | 來源出版物: | Journal of Applied Physiology | 摘要: | We previously reported that genetically obese mice exhibit innate airway hyperresponsiveness (AHR) and enhanced ozone (O3)-induced pulmonary inflammation. Such genetic deficiencies in mice are rare in humans, and they may not be representative of human obesity. Thus the purpose of this study was to determine the pulmonary phenotype of mice with diet-induced obesity (DIO), which more closely mimics the cause of human obesity. Therefore, wild-type C57BL/6 mice were reared from the time of weaning until at least 30 wk of age on diets in which either 10 or 60% of the calories are derived from fat in the form of lard. Body mass was ?40% greater in mice fed 60 vs. 10% fat diets. Baseline airway responsiveness to intravenous methacholine, measured by forced oscillation, was greater in mice fed 60 vs. 10% fat diets. We also examined lung permeability and inflammation after exposure to room air or O3 (2 parts/million for 3 h), an asthma trigger. Four hours after the exposure ended, O3-induced increases in bronchoalveolar lavage fluid protein, interleukin-6, KC, macrophage inflammatory protein-2, interferon-γ-inducible protein-10, and eotaxin were greater in mice fed 60 vs. 10% fat diets. Innate AHR and augmented responses to O3 were not observed in mice raised from weaning until 20-22 wk of age on a 60% fat diet. These results indicate that mice with DIO exhibit innate AHR and enhanced O3-induced pulmonary inflammation, similar to genetically obese mice. However, mice with DIO must remain obese for an extended period of time before this pulmonary phenotype is observed. Copyright ? 2008 the American Physiological Society. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-49649113435&doi=10.1152%2fjapplphysiol.00075.2008&partnerID=40&md5=013162097069278d3932148ff13b96bc https://scholars.lib.ntu.edu.tw/handle/123456789/524940 |
ISSN: | 8750-7587 | DOI: | 10.1152/japplphysiol.00075.2008 | SDG/關鍵字: | chemokine; eotaxin; gamma interferon inducible protein 10; interleukin 6; macrophage inflammatory protein 2; methacholine; ozone; protein kinase C; autacoid; bronchoconstricting agent; lard; methacholine chloride; ozone; airway resistance; animal experiment; animal model; animal tissue; article; body mass; controlled study; cytokine production; diet; female; lung lavage; lung resistance; male; mouse; nonhuman; obesity; pneumonia; priority journal; animal; body weight; breathing mechanics; bronchus hyperreactivity; C57BL mouse; chemically induced disorder; chemistry; cytology; disease model; dose response; drug effect; fat intake; inhalation test; intravenous drug administration; lung compliance; lung edema; metabolism; obesity; pathophysiology; phenotype; pneumonia; Airway Resistance; Animals; Body Weight; Bronchial Hyperreactivity; Bronchial Provocation Tests; Bronchoalveolar Lavage Fluid; Bronchoconstrictor Agents; Dietary Fats; Disease Models, Animal; Dose-Response Relationship, Drug; Female; Inflammation Mediators; Injections, Intravenous; Lung Compliance; Male; Methacholine Chloride; Mice; Mice, Inbred C57BL; Obesity; Ozone; Phenotype; Pneumonia; Pulmonary Edema; Respiratory Mechanics |
顯示於: | 醫學系 |
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