早期营养过剩加重哮喘小鼠肺组织炎症和气道反应性  

Neonatal overfeeding worsen the pulmonary inflammation and airway hyperresponsiveness in asthma mice

作　　者：王冬娟[1] 黄英[1] 肖晓秋[1] 崔欢欢[1] 宋晔[1] 刘丹[1] 叶泽慧[1] 

机构地区：[1]重庆医科大学附属儿童医院呼吸中心儿童发育疾病研究教育部重点实验室儿科学重庆市重点实验室重庆市儿童发育重大疾病诊治与预防国际科技合作基地,400014

出　　处：《免疫学杂志》2014年第6期508-511,共4页Immunological Journal

摘　　要：目的通过早期营养过剩建立肥胖小鼠模型,探讨肥胖对哮喘小鼠肺部炎症及气道反应性的影响。方法采用小窝喂养的方法建立早期营养过剩肥胖小鼠模型,实验组采用鸡卵白蛋白(OVA)腹腔注射致敏及雾化吸入激发的方法建立哮喘模型,对照组采用等量生理盐水腹腔注射及雾化吸入,分组为肥胖哮喘组、单纯哮喘组、单纯肥胖组和正常对照组。最后一次激发后行肺功能测定检测肥胖对哮喘气道反应性的影响,行肺泡灌洗术分析灌洗液中炎症细胞总数和分类、肺组织HE染色检测肥胖对哮喘炎症的影响。结果 1)哮喘小鼠气道反应性明显高于对照组,肥胖哮喘小鼠较单纯肥胖组和哮喘组小鼠气道反应性明显升高(P均<0.05)。2)与哮喘组和肥胖组相比,肥胖哮喘组灌洗液炎症细胞总数和分类炎症细胞明显升高(P均<0.05),与对照组相比,单纯肥胖组炎症细胞总数和巨噬细胞增多(P均<0.05),其他炎症细胞无差异(P均>0.05)。3)与肥胖组相比,肥胖哮喘组支气管周围和肺泡间隙炎症细胞明显增多(P均<0.05),与哮喘组相比,仅表现为支气管周围炎症细胞增多(P<0.05)。结论早期营养过剩诱导的肥胖小鼠可明显增加哮喘小鼠气道反应性及肺组织炎症。This study designed to explore the effect of neonatal overfeeding-induced obesity on airway inflammation and responsiveness in asthma mice. Neonatal overfeeding induced obesity model was established by reducing the litter size; asthma model was founded by sensitization and challenge with ovalbumin intraperitoneal injection and aerosol respectively, while control group were treated with saline instead. The groups were defined as obese asthma group, asthma group, obese group, and control group. Then airway resistance was performed after the last OVA stimulation to detect the effect of obesity on airway responsiveness. Furthermore, bronchoalveolar lavage fluid （BALF） cell count and lung tissue hematoxylin-eosin stain （H＆E） were implemented to identify the role of obesity in airway inflammation. In asthmatic mice, airway responsiveness was higher than that in controls, while obese asthma mice showed a greater degree of airway responsiveness when compared with obese mice and control mice （P〈0.05）. Total and classified cells in BALF of obese asthma mice revealed a remarkable increase compared with obese mice and asthma mice （P〈0.05）. Except for the total cells and macrophages displayed a significant difference between obese mice and controls （P 〈 0.05）, there was no other difference in cell count between these two groups （P 〉 0.05）. Furthermore, Hematoxylin-Eosin stain indicated that inflammatory cells recruit to the peri-bronchial and interstitial alveolar obviously in obese asthma mice than that in obese mice （P〈 0.05）, but obese asthma mice just exhibited more cell accumulation in perihronchial when compared with asthma mice. All these results indicated that neonatal overfeeding-induced obesity can augment the airway inflammation and responsiveness in asthma mice.

关 键 词：早期营养过剩 肥胖 哮喘 气道高反应性 肺组织炎症 

分 类 号：R589.2[医药卫生—内分泌] R562.25[医药卫生—内科学]