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粘蛋白1的物理屏障作用与其抑制呼吸道合胞病毒诱导呼吸道炎症无关 被引量:1

Mucin 1 in respiratory syncytial virus infection is independent on its airway physical barrier function for anti-inflammatory effect
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摘要 目的探讨呼吸道合胞病毒(RSV)感染呼吸道上皮细胞后表达上调的粘蛋白1(MUC1)是否可以通过物理屏障作用阻止RSV接近并感染呼吸道上皮细胞,进而抑制炎症反应。方法我们通过向两种呼吸道上皮细胞系(A549和HEp-2)中转染MUC1真核表达载体pcDNA3.1-MUC1的方法过表达MUC1,再应用相同感染复数的RSV分别感染过表达MUC1和转染对照质粒pcDNA3.1的呼吸道上皮细胞,最后比较感染两种细胞内RSV的滴度。结果 RSV成功感染体外培养的两种呼吸道上皮细胞,且RSV在HEp-2细胞内形成的空斑较A549细胞内形成的空斑易于计数。过表达MUC1和转染对照质粒pcDNA3.1的呼吸道上皮细胞内病毒滴度无显著差异。结论呼吸道上皮细胞过表达的MUC1不能抑制RSV接近并感染呼吸道上皮细胞,即MUC1不是通过物理屏障作用抑制RSV诱导炎症反应。 To investigate whether the mucin 1(MUC1) induced by respiratory syncytial virus(RSV) infection can prevent RSV from accessing and infecting airway epithelial cells thereby inhibiting the inflammatory response,we transfected two kinds of airway epithelial cells(A549 and HEp-2) with eukaryotic expression vector of pcDNA3.1-MUC1 to overexpress MUC1,and then used RSV to infect the MUC1-overexpressed airway epithelial cells and normal airway epithelial cells transfected with pcDNA3.1,and finally compared the RSV titer in two kinds of cells.Our results showed that RSV infected the two kinds of airway epithelial cells in vitro successfully,and the plaque in HEp-2 cells caused by RSV was easier to count than in A549 cells.It was found that there was no significant difference of RSV titer between the airway epithelial cells transfected with pcDNA3.1-MUC1 and control plasmid pcDNA3.1 in two kinds of airway epithelial cells.We conclude that overexpressed MUC1 in airway epithelial cells could not prevent RSV from accessing and infecting airway epithelial cells,suggesting that MUC1's inhibition of RSV-induced inflammation is not through its physical barrier function.
出处 《中国人兽共患病学报》 CAS CSCD 北大核心 2012年第6期549-554,565,共7页 Chinese Journal of Zoonoses
基金 国家自然科学基金青年基金(No.81100008) 广东省高校优秀青年创新人才培育项目(No.LYM10048)资助~~
关键词 呼吸道合胞病毒 呼吸道上皮细胞 粘蛋白1 抑制炎症 物理屏障 respiratory syncytial virus airway epithelial cells mucin 1 anti-inflammatory physical barriers
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参考文献25

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