Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Respir Physiol Neurobiol. 2011 Jul 31;177(2):141-8. doi: 10.1016/j.resp.2011.03.019. Epub 2011 Mar 29.
The impact of obesity on the inflammatory process has been described in asthma, however little is known about the influence of diet-induced obesity on lung remodeling. For this purpose, 56 recently weaned A/J mice were randomly divided into 2 groups. In the C group, mice were fed a standard chow diet, while OB animals received isocaloric high-fat diet to reach 1.5 of the mean body weight of C. After 12 weeks, each group was further randomized to be sensitized and challenged with ovalbumin (OVA) or saline. Twenty-four hours after the last challenge, collagen fiber content in airways and lung parenchyma, the volume proportion of smooth muscle-specific actin in alveolar ducts and terminal bronchiole, and the number of eosinophils in bronchoalveolar lavage fluid were higher in OB-OVA than C-OVA. In conclusion, diet-induced obesity enhanced lung remodeling resulting in higher airway responsiveness in the present experimental chronic allergic asthma.
肥胖对炎症过程的影响在哮喘中已有描述，但对于饮食诱导的肥胖对肺重塑的影响知之甚少。为此，我们将 56 只最近断奶的 A/J 小鼠随机分为 2 组。在 C 组中，小鼠喂食标准的饲料，而 OB 组动物则喂食等热量高脂肪饮食，使其体重达到 C 组的 1.5 倍。12 周后，每组进一步随机分为卵清蛋白（OVA）或盐水致敏和激发组。最后一次激发后 24 小时，OB-OVA 组气道和肺实质中的胶原纤维含量、肺泡导管和终末细支气管中平滑肌特异性肌动蛋白的体积比例、以及支气管肺泡灌洗液中的嗜酸性粒细胞数量均高于 C-OVA 组。总之，饮食诱导的肥胖增强了肺重塑，导致本实验性慢性变应性哮喘的气道高反应性增加。
