Jenield J D'abreo, Emily K Chivers, Peter B Noble, Luke J Berry, Rachel R Huxley, Arthur Bill W Musk, Peter J Franklin, Benjamin J Mullins, Katherine R Landwehr, Alexander N Larcombe
{"title":"电子烟使用对成年BALB/c小鼠哮喘严重程度的影响。","authors":"Jenield J D'abreo, Emily K Chivers, Peter B Noble, Luke J Berry, Rachel R Huxley, Arthur Bill W Musk, Peter J Franklin, Benjamin J Mullins, Katherine R Landwehr, Alexander N Larcombe","doi":"10.1113/EP092959","DOIUrl":null,"url":null,"abstract":"<p><p>Electronic cigarettes (e-cigarettes) are often perceived to be a less harmful alternative to tobacco cigarettes. Potentially due to this perception, they are used by people with pre-existing respiratory conditions, such as asthma, who otherwise would not smoke. Despite this, there are few studies exploring the health effects of e-cigarette use on pre-existing asthma. In this study, a house dust mite-induced allergic-airways disease phenotype was generated in adult BALB/c mice over 7 weeks. For the last 2 weeks of this period, mice were also exposed to either medical air, or tobacco smoke or e-cigarette aerosol (with or without nicotine) for 2 h/day. Twenty-four hours later, respiratory parameters including lung volume/function and responsiveness to methacholine were assessed. Biological samples were taken for analysis of pulmonary cellular inflammation and mediator levels, serum IgE and lung/airway structure. There were complex effects of exposure on respiratory outcomes. For example, tobacco smoke-exposed mice of both sexes were the most responsive to methacholine but had suppressed total cellular and eosinophilic inflammation. Female e-cigarette aerosol-exposed mice had impaired parenchymal mechanics at functional residual capacity compared with tobacco smoke-exposed mice, irrespective of nicotine. Interferon γ levels were suppressed in both e-cigarette-exposed groups. There was no effect of any exposure on IgE or lung structural parameters. E-cigarette aerosol exposure exacerbated aspects of an allergic airways disease phenotype in mice. This suggests that asthmatics should exercise increased caution if thinking of using e-cigarettes.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8000,"publicationDate":"2025-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The effects of e-cigarette use on asthma severity in adult BALB/c mice.\",\"authors\":\"Jenield J D'abreo, Emily K Chivers, Peter B Noble, Luke J Berry, Rachel R Huxley, Arthur Bill W Musk, Peter J Franklin, Benjamin J Mullins, Katherine R Landwehr, Alexander N Larcombe\",\"doi\":\"10.1113/EP092959\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Electronic cigarettes (e-cigarettes) are often perceived to be a less harmful alternative to tobacco cigarettes. Potentially due to this perception, they are used by people with pre-existing respiratory conditions, such as asthma, who otherwise would not smoke. Despite this, there are few studies exploring the health effects of e-cigarette use on pre-existing asthma. In this study, a house dust mite-induced allergic-airways disease phenotype was generated in adult BALB/c mice over 7 weeks. For the last 2 weeks of this period, mice were also exposed to either medical air, or tobacco smoke or e-cigarette aerosol (with or without nicotine) for 2 h/day. Twenty-four hours later, respiratory parameters including lung volume/function and responsiveness to methacholine were assessed. Biological samples were taken for analysis of pulmonary cellular inflammation and mediator levels, serum IgE and lung/airway structure. There were complex effects of exposure on respiratory outcomes. For example, tobacco smoke-exposed mice of both sexes were the most responsive to methacholine but had suppressed total cellular and eosinophilic inflammation. Female e-cigarette aerosol-exposed mice had impaired parenchymal mechanics at functional residual capacity compared with tobacco smoke-exposed mice, irrespective of nicotine. Interferon γ levels were suppressed in both e-cigarette-exposed groups. There was no effect of any exposure on IgE or lung structural parameters. E-cigarette aerosol exposure exacerbated aspects of an allergic airways disease phenotype in mice. 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The effects of e-cigarette use on asthma severity in adult BALB/c mice.
Electronic cigarettes (e-cigarettes) are often perceived to be a less harmful alternative to tobacco cigarettes. Potentially due to this perception, they are used by people with pre-existing respiratory conditions, such as asthma, who otherwise would not smoke. Despite this, there are few studies exploring the health effects of e-cigarette use on pre-existing asthma. In this study, a house dust mite-induced allergic-airways disease phenotype was generated in adult BALB/c mice over 7 weeks. For the last 2 weeks of this period, mice were also exposed to either medical air, or tobacco smoke or e-cigarette aerosol (with or without nicotine) for 2 h/day. Twenty-four hours later, respiratory parameters including lung volume/function and responsiveness to methacholine were assessed. Biological samples were taken for analysis of pulmonary cellular inflammation and mediator levels, serum IgE and lung/airway structure. There were complex effects of exposure on respiratory outcomes. For example, tobacco smoke-exposed mice of both sexes were the most responsive to methacholine but had suppressed total cellular and eosinophilic inflammation. Female e-cigarette aerosol-exposed mice had impaired parenchymal mechanics at functional residual capacity compared with tobacco smoke-exposed mice, irrespective of nicotine. Interferon γ levels were suppressed in both e-cigarette-exposed groups. There was no effect of any exposure on IgE or lung structural parameters. E-cigarette aerosol exposure exacerbated aspects of an allergic airways disease phenotype in mice. This suggests that asthmatics should exercise increased caution if thinking of using e-cigarettes.
期刊介绍:
Experimental Physiology publishes research papers that report novel insights into homeostatic and adaptive responses in health, as well as those that further our understanding of pathophysiological mechanisms in disease. We encourage papers that embrace the journal’s orientation of translation and integration, including studies of the adaptive responses to exercise, acute and chronic environmental stressors, growth and aging, and diseases where integrative homeostatic mechanisms play a key role in the response to and evolution of the disease process. Examples of such diseases include hypertension, heart failure, hypoxic lung disease, endocrine and neurological disorders. We are also keen to publish research that has a translational aspect or clinical application. Comparative physiology work that can be applied to aid the understanding human physiology is also encouraged.
Manuscripts that report the use of bioinformatic, genomic, molecular, proteomic and cellular techniques to provide novel insights into integrative physiological and pathophysiological mechanisms are welcomed.