Nebraska Medical Center, Univ. of Nebraska Medical Ctr., Omaha, NE 68198-5910, USA.
Am J Physiol Lung Cell Mol Physiol. 2012 Feb 1;302(3):L308-15. doi: 10.1152/ajplung.00077.2011. Epub 2011 Nov 23.
There is very limited knowledge about the effects of alcohol on airway hyperresponsiveness and inflammation in asthma. Historical accounts of alcohol administration to patients with breathing problems suggest that alcohol may have bronchodilating properties. We hypothesized that alcohol exposure will alter airway hyperresponsiveness (AHR) and pulmonary inflammation in a mouse model of allergic asthma. To test this hypothesis, BALB/c mice were fed either 18% alcohol or water and then sensitized and challenged with ovalbumin (OVA). AHR was assessed by means of ventilation or barometric plethysmography and reported as either total lung resistance or enhanced pause, respectively. Airway inflammation was assessed by total and differential cell counts in bronchoalveolar lavage fluid (BALF), cytokine levels in BALF, lung histology, and serum immunoglobulin E (IgE) levels. Alcohol feeding significantly blocked methacholine-induced increases in AHR compared with water-fed controls. Alcohol feeding significantly reduced total cell numbers (64%) as well as the number of eosinophils (84%) recruited to the lungs of these mice. Modest changes in lung pathology were also observed. Alcohol exposure led to a reduction of IgE in the serum of the EtOH OVA mice. These data demonstrate that alcohol exposure blunts AHR and dampens allergic airway inflammation indices in allergic mice and suggest that there may be an important role for alcohol in the modulation of asthma. These data provide an in vivo basis for previous clinical observations in humans substantiating the bronchodilator properties of alcohol and for the first time demonstrates an alcohol-induced reduction of allergic inflammatory cells in a mouse model of allergic asthma.
关于酒精对哮喘气道高反应性和炎症的影响，我们的了解非常有限。历史上有关于给有呼吸问题的患者使用酒精的记载，表明酒精可能具有支气管扩张的特性。我们假设，酒精暴露会改变过敏性哮喘小鼠模型中的气道高反应性（AHR）和肺部炎症。为了验证这一假设，我们给 BALB/c 小鼠喂食 18%的酒精或水，然后用卵清蛋白（OVA）致敏和激发它们。通过通气或气压描记法评估 AHR，并分别报告为总肺阻力或增强暂停。通过支气管肺泡灌洗液（BALF）中的总细胞计数和差异细胞计数、BALF 中的细胞因子水平、肺组织学和血清免疫球蛋白 E（IgE）水平评估气道炎症。与饮水对照组相比，酒精喂养显著阻断了乙酰甲胆碱引起的 AHR 增加。酒精喂养还显著降低了这些小鼠肺部的总细胞数（64%）和嗜酸性粒细胞数（84%）。还观察到肺病理学的轻微变化。酒精暴露导致 EtOH-OVA 小鼠血清中的 IgE 减少。这些数据表明，酒精暴露可减轻过敏性小鼠的 AHR 并抑制过敏性气道炎症指标，提示酒精在哮喘的调节中可能发挥重要作用。这些数据为先前在人类中观察到的酒精的支气管扩张特性提供了体内依据，并首次证明了在过敏性哮喘的小鼠模型中，酒精可诱导过敏炎症细胞减少。
