Mechanisms of exacerbation of asthma induced by RS virus infection and it's regulation due to drugs

人呼吸道合胞病毒（RSV）感染在婴儿期和幼儿期可引起急性细支气管炎并加重支气管哮喘。嗜酸性粒细胞浸润可能导致呼吸道合胞病毒感染的气道阻塞。我们假设RSV影响嗜酸性粒细胞功能。通过化学发光检测超氧阴离子(O（2)(-)）的生成来评估嗜酸性粒细胞的活化。流式细胞术检测CD11b在嗜酸性粒细胞中的表达。虽然RSV不会诱导静息的嗜酸性粒细胞生成O(2)(-)，但RSV通过血小板活化因子（PAF）诱导嗜酸性粒细胞生成O(2)（-）。持续搅拌以防止嗜酸性粒细胞粘附在试管表面或用抗cd18抗体预处理细胞均可显著抑制增强，这表明RSV对嗜酸性粒细胞的刺激作用依赖于通过β(2)-整合素的细胞粘附。事实上，RSV通过嗜酸性粒细胞增强了paf诱导的CD11b表达。这些发现提示RSV增强嗜酸性粒细胞CD11b表达和PAF诱导的O(2)（-）生成。因此，RSV感染可能通过增强嗜酸性粒细胞释放介质而加重气道炎症。

Human respiratory syncytial virus (RSV) infection in infancy and early childhood causes acute bronchiolitis and exacerbates bronchial asthma. Eosinophil infiltration may contribute to airway obstruction in RSV infection. We hypothesized that RSV affects eosinophil function. Eosinophil activation was evaluated by chemiluminescent detection of superoxide anion (O(2)(-)) generation. Expression of CD11b on eosinophils was determined by flow cytometry. Although RSV did not induce O(2)(-) generation by resting eosinophils, RSV enhanced O(2)(-) generation of eosinophils primed with platelet-activating factor (PAF). Enhancement was significantly inhibited by either continuous agitation to prevent eosinophil adhesion to test tube surfaces or by pretreating cells with anti-CD18 antibody, suggesting that the stimulatory effects of RSV on eosinophils depend on cell adhesion via beta(2)-integrins. In fact, RSV enhanced PAF-induced CD11b expression by eosinophils. These findings suggest that RSV enhances eosinophil CD11b expression and O(2)(-) generation induced by PAF. Thus, RSV infection may exacerbate airway inflammation by enhancing mediator release from eosinophils.