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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 pathogenesis of airway inflammation and recurrent wheezing after recurrent respiratory virus infection after respiratory syncytial virus (RSV) infection. Methods Sixty-four female BALB / c mice aged 6-8 weeks were randomly divided into control group, RSV group, Poly (I: C) group and RSV + Poly (I: C) group (n = 16). Bronchoalveolar lavage fluid (BALF) of each group was collected, the total number of cells in the BALF was counted, the number of cells was counted, hematoxylin and eosin (HE) staining was used to observe the pathological lung injury, the airway responsiveness (AHR) The levels of IFN-γ, IL-4, IL-13, MMP-9 and TIMP-1 in BALF were measured. Results The total number of airway inflammatory cells infiltration and AHR in RSV + Poly (I: C) group were significantly higher than those in other three groups (P <0.05). Compared with control group and RSV group, the pathological damage of lung tissue of RSV + Poly (I: C) group was more severe than that of control group and RSV group (P <0.01) 4 and TIMP-1 were significantly lower than RSV group (P <0.01). Conclusions The re-infection of virus after RSV infection may cause imbalance of MMP-9 / TIMP-1 expression and aggravate airway inflammation.