【打印本页】 【下载PDF全文】 【HTML】 查看/发表评论下载PDF阅读器关闭

←前一篇|后一篇→

过刊浏览    高级检索

本文已被:浏览 2117次   下载 1842 本文二维码信息
码上扫一扫!
呼吸道合胞病毒感染加重哮喘模型小鼠气道炎症及气道阻力的观察
景晓平1,程伟伟1,刘芳2,杨华2,何丽1*
0
(1. 上海市儿童医院, 上海交通大学附属儿童医院中医科, 上海 200040;
2. 复旦大学附属公共卫生临床中心科学研究部, 上海 202508
*通信作者)
摘要:
目的 探讨呼吸道合胞病毒(RSV)感染加重哮喘模型小鼠气道炎症及气道阻力变化的影响。 方法 6~8周龄雄性BALB/c小鼠30只,随机分为空白组、卵清蛋白(OVA)组(哮喘模型组)、OVA/RSV组(RSV+哮喘模型组),每组10只。OVA组用OVA致敏和激发;OVA/RSV组在OVA 致敏后隔日用RSV滴鼻,连续3次,复制急性病毒感染哮喘模型;空白组予等量PBS。末次激发24 h后,用小鼠动物呼吸机(Buxco RC系统)检测小鼠气道阻力;收集支气管肺泡灌洗液(BALF)进行细胞学分析;留取肺组织进行H-E染色、PAS染色、VG染色,观察肺组织炎症反应。 结果 OVA组小鼠肺组织有炎性细胞浸润,气道可见黏液分泌物,气道周围可见胶原增生。OVA/RSV组小鼠肺组织有明显炎性细胞浸润,肺泡腔明显狭窄,毛细血管扩张充血,气道可见明显黏液分泌物,气道周围胶原增生明显。OVA组、OVA/RSV组肺功能和BALF嗜酸粒细胞比例(EOS%)与空白组相比差异有统计学意义 (P<0.05,P<0.01),OVA/RSV组气道阻力及BALF中EOS%与OVA组相比差异有统计学意义(P<0.05)。 结论 RSV感染能明显加重哮喘模型小鼠肺部组织炎症反应,同时使小鼠气道阻力明显增高。
关键词:  呼吸道合胞病毒  哮喘  气道炎症  气道阻力
DOI:10.3724/SP.J.1008.2015.01284
投稿时间:2015-04-29修订日期:2015-10-20
基金项目:国家自然科学基金青年基金(81303005),上海市自然科学基金(12ZR1425700).
Aggravated airway inflammation and resistance in a respiratory syncytial virus infected murine asthma model
JING Xiao-ping1,CHENG Wei-wei1,LIU Fang2,YANG Hua2,HE Li1*
(1. Department of TCM, Shanghai Children's Hospital, Shanghai Jiaotong University, Shanghai 200040, China;
2. Department of Scientific Research, Public Health Clinical Center Affiliated to Fudan University, Shanghai 202508, China
*Corresponding author.)
Abstract:
Objective To explore the role of respiratory syncytial virus (RSV) infection in aggravating airway inflammation and airway resistance in murine asthma model. Methods A total of 30 6-8-week-old male BALB/c mice were equally divided into three groups randomly: the control group, ovalbumin (OVA) group (asthma group), and respiratory syncytial virus (RSV)/OVA group (RSV+asthma group). In OVA group, murine asthma model was established using an OVA sensitization; in OSV/RSV group, mice were firstly sensitized by OVA and subsequently infected with RSV intranasally for three times to make acute viral infection asthma model; and in control group, the mice received equal volume of PBS treatment. Twenty-four hours after the last challenge, the airway resistance was evaluated by mouse ventilator (Buxco RC). Inflammatory cell infiltration was measured in bronchoalveolar lavage fluid (BALF). Pulmonary tissue samples were collected and stained with H-E, PAS or VG to observe inflammation of pulmonary tissues. Results Pulmonary tissue of mice in OVA group had inflammatory cell infiltration, airway mucus secretions were visible, and collagen was seen around the airway. Pulmonary tissue of mice in OVA/RSV group had significant inflammatory cell infiltration, alveolar stenosis, telangiectasia congestion, airway mucus secretions and collagen deposition. Lung function and the proportion of BALF eosinophils (EOS%) in OVA group and OVA/RSV group were significantly different from that of the control group (P<0.05,P<0.01). Airway resistance and the EOS% in OVA/RSV group were significantly different from those of the OVA group (P<0.05). Conclusion RSV infection can aggravate the airway inflammation and result in airway resistance in murine asthma model.
Key words:  respiratory syncytial viruses  asthma  airway inflammation  airway resistance