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地塞米松对呼吸道合胞病毒感染小鼠肺泡巨噬细胞分化的影响 被引量:1

Influence of dexamethasone on alveolar macrophage differentiation in respiratory syncytial virus infected mice
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摘要 目的观察地塞米松(dexamethasone,DEX)对小鼠骨髓来源的巨噬细胞(respiratory syncytial virus,BMDM)及呼吸道合胞病毒(RSV)感染小鼠的肺泡巨噬细胞分化的影响。方法体外诱导培养M1型BMDM,鉴定其表型,观察DEX对巨噬细胞转录因子和细胞因子表达的影响;以RSV感染小鼠,同时给予DEX,观察DEX对小鼠肺泡巨噬细胞转录因子和细胞因子表达的影响。结果 DEX能抑制M1型BMDM及RSV感染小鼠的肺泡巨噬细胞中IL-6、IL-12、i NOS和IRF5的表达,并促进IL-10、Arginase-1和IRF4的表达,使M1型巨噬细胞向M2型转化。结论 DEX可在体内外将M1型巨噬细胞转化为M2型巨噬细胞,抑制炎症反应,这可能是DEX治疗RSV感染的作用机制之一。 Objective To observe the influence of dexamethasone on M1 BMDM and alveolar macrophage differentiation in respiratory syncytial virus( RSV) infected mice. Methods Culture M1 BMDM and identify its phenotype,observe the effect of DEX on its transcription factors and cytokines; In RSV infected mice,observe the influence of DEX on the transcription factors and cytokines of alveolar macrophage. Results DEX can inhibit IL-6,IL-12,i NOS and IRF5 expression,but promote IL-10,Arginase-1 and IRF4 expression in M1 BMDM and alveolar macrophages of RSV infected mice,made M1 macrophages transform to M2 macrophages. Conclusion DEX can transform M1 macrophages to M2 macrophages in vivo and in vitro,and inhibit inflammation,this may be one of the mechanism of DEX in the treatment of RSV infection.
出处 《中国生化药物杂志》 CAS 2016年第8期27-30,共4页 Chinese Journal of Biochemical Pharmaceutics
基金 湖北省自然科学基金(2015CFB621)
关键词 地塞米松 呼吸道合胞病毒 巨噬细胞 dexamethasone respiratory syncytial virus macrophage
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  • 1Joseph BD, Helene FR. Respiratory syncytial virus infection: immune response, immunopathogenesis, and treatment [ J ]. Clin Microbiol Rev, 1999,12:298-309.
  • 2Locati M, Mantovani A, Sica A. Macrophage activation and polarization as an adaptive component of innate immunity[ J ]. Adv Immunol,2013, 120 : 163-184.
  • 3Tugal D, Liao X, Jain MK. Transcriptional control of maerophage polarization [ J ]. Arterioseler Thromb Vasc Biol, 2013, 33 ( 6 ) : 1135-1144.
  • 4Krausgruber T, Blazek K, Smallie T, et al. IRF5 promotes inflammatory macrophage polarization and TH1-TH17 responses [ J ]. Nat Immunol, 2011,12(3) :231-238.
  • 5Xu H, Zhu J, Smith S, et al. Noteh-RBP-J signaling regulates the transcription factor IRF8 to promote inflammatory maerophage polarization [ J ]. Nat Immunol,2012,13 ( 7 ) :642-650.
  • 6Date D, Das R, Narla G, et al. Kruppel-like transcription factor 6regulates inflammatory macrophage polarization[ J]. J Biol Chem,2014, 285 ( 15 ) : 10318-10329.
  • 7Liao X, Sharma N, Kapadia F, et al. Krtippel-like factor 4 regulates macrophage polarization [ J ]. J Clin Invest ,2011,121 (7) :2736-2749.
  • 8Satoh T, Takeuehi O, Vandenbon A, et al. The Jmjd3-Irf4 axis regulates M2 macrophage polarization and host responses against helminth infection[ J]. Nat Immunol,2010,11:936-944.
  • 9Midge JL, Mehraj V, Capo C. Macrophage polarization and bacterial infections [ J ]. Curt Opin Infect Dis,2011,24 ( 3 ) :230-234.
  • 10Huang SH, Cao X J, Wei W. Melatonin decreases TLR3-mediated inflammatory factor expression via inhibition of NF-kappa B activation in respiratory syncytial virus-infected RAW264.7 macrophages [ J ]. J Pineal Res,2008,45( 1 ) :93-100.

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