Jiang Xiong-Bin, Huang Mao, Cui Xue-Fan, Zhu Yi, Yin Kai-Sheng, Yao Kun
Department of Respiratory Disease, the First Affiliated Hospital of Nanjing Medical University, Nanjing, P.R. China.
Exp Lung Res. 2012 Nov;38(9-10):453-62. doi: 10.3109/01902148.2012.723240. Epub 2012 Sep 10.
Much evidence suggests that respiratory syncytial virus (RSV) infection prolongs airway hyperresponsiveness (AHR) and exacerbates asthma by enhancing airway inflammation. However, the characteristic of airway inflammation and kinetics of airway dysfunction occurred in the central and peripheral airways were not fully delineated. The objective of this study was to investigate the effect of RSV on the allergic airway inflammation in different size airways and to elucidate its possible mechanism. Using a murine model of prior ovalbumin (OVA) sensitization and subsequent RSV challenge, lung resistance (R(L)), and dynamic compliance (Cdyn) was conducted by barometric whole-body plethysmography. Histological examinations were carried out. Differential cells count in bronchoalveolar lavage (BAL) fluid, serum anti-OVA IgE, and IgG1 were measured. Cytokine mRNA expression in lung tissue were determined. RSV triggered a significant increase in R(L) and reduction in Cdyn, as well as greatly prolonged the recovery of Cdyn more than that of R(L) in OVA-sensitized mice. Also, RSV resulted in more severe peripheral airway inflammation which exhibit as globe cell hyperplasia and CD8+ T cell infiltration. Furthermore, the number of lymphocytes, neutrophils and macrophages in BAL fluid, serum anti-OVA IgE and IgG1 were remarkably increased. Additionally, mice increased relative expression of cytokines IL-4, IL-13, and IFN-γ, but not IL-5, IL-17, and IL-17F. These findings demonstrated that RSV could selectively affect pathologic processes that contribute to altered airway function in the central and peripheral airways in OVA-sensitized mice. These processes may be involved in goblet cell hyperplasia and CD8+ T cell infiltration in peripheral airways.
许多证据表明，呼吸道合胞病毒（RSV）感染会延长气道高反应性（AHR），并通过加剧气道炎症来加重哮喘。然而，中央气道和外周气道中发生的气道炎症特征及气道功能障碍的动力学尚未完全阐明。本研究的目的是探讨RSV对不同大小气道中过敏性气道炎症的影响，并阐明其可能机制。利用卵清蛋白（OVA）致敏并随后进行RSV攻击的小鼠模型，通过气压式全身体积描记法测量肺阻力（R(L)）和动态顺应性（Cdyn）。进行了组织学检查。测量支气管肺泡灌洗（BAL）液中的差异细胞计数、血清抗OVA IgE和IgG1。测定肺组织中细胞因子mRNA表达。RSV导致OVA致敏小鼠的R(L)显著增加、Cdyn降低，并且Cdyn的恢复时间比R(L)大大延长。此外，RSV导致更严重的外周气道炎症，表现为杯状细胞增生和CD8+ T细胞浸润。此外，BAL液中的淋巴细胞、中性粒细胞和巨噬细胞数量、血清抗OVA IgE和IgG1显著增加。另外，小鼠细胞因子IL-4、IL-13和IFN-γ的相对表达增加，但IL-5、IL-17和IL-17F未增加。这些发现表明，RSV可选择性影响OVA致敏小鼠中央气道和外周气道中导致气道功能改变的病理过程。这些过程可能与外周气道中的杯状细胞增生和CD8+ T细胞浸润有关。
