摘要
目的探讨呼吸道合胞病毒（RSV）感染后再发呼吸道病毒感染时诱发气道炎症及反复喘息的致病机制。方法 64只6-8周雌性BALB/c小鼠随机分为对照组、RSV组、Poly（I：C）组及RSV＋Poly（I：C）组（n=16）。收集各组肺泡灌洗液（BALF）,计数BALF中细胞总数及分类计数,苏木精-伊红（HE）染色观察肺部病理损伤,检测小鼠气道反应性（AHR）,ELISA法检测BALF中IFN-γ、IL-4、IL-13、基质金属蛋白酸9（MMP-9）及基质金属蛋白酶抑制物-1（TIMP-1）水平。结果 RSV＋Poly（I：C）组小鼠的气道炎症细胞浸润总数及AHR较其他3组显著增高（P〈0.05）。RSV＋Poly（I：C）组小鼠的肺组织病理损伤较对照组及RSV组加重（P〈0.01）;BALF中MMP-9水平较其他3组明显升高（P〈0.05）,IL-4及TIMP-1显著低于RSV组（P〈0.01）。结论 RSV感染后病毒再感染可能引起MMP-9/TIMP-1表达失衡,加重气道炎症反应。
Objective To investigate the pathogenic mechanisms of airway inflammation and recurrent wheezing induced by recurrent respiratory virus infection after respiratory syncytial virus（RSV）infection.Methods Sixtyfour female BALB/c mice（aged 6-8 weeks）were randomly divided into four groups：control,RSV,Poly（I：C）,and RSV＋Poly（I：C）（n=16 each）.The bronchoalveolar lavage fluid（BALF）was collected on the 3rd day after Poly（I：C）administration,and the total cell number and differential counts in BALF were determined.Hematoxylin-eosin staining was used to observe pulmonary pathological changes.The airway responsiveness was detected.ELISA was used to measure the levels of interferon-γ（IFN-γ）,interleukin-4（IL-4）,interleukin-13（IL-13）,matrix metallopeptidase-9（MMP-9）,and tissue inhibitor of metalloproteinase-1（TIMP-1）in BALF.Results Compared with the other three groups,the RSV＋Poly（I：C）group had significant increases in the total number of inflammatory infiltrating cells in the airway,airway responsiveness,and MMP-9 level in BALF（P〈0.05）.The RSV＋Poly（I：C）group showed more severe pulmonary tissue injuries compared with the control and RSV groups（P〈0.01）.Compared with the RSV group,the RSV＋Poly（I：C）group showed significant reductions in the levels of IL-4 and TIMP-1 in BALF（P〈0.01）.Conclusions Viral re-infection in the late stage of RSV infection may cause an imbalance of MMP-9/TIMP-1 expression and thus contribute to aggravated airway inflammation.
出处
《中国当代儿科杂志》
CAS
CSCD
北大核心
2016年第5期455-459,共5页
Chinese Journal of Contemporary Pediatrics
基金
国家自然科学基金(81170010
81470208)
