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The TLR4 antagonist Eritoran protects mice from lethal influenza infection

机译:TLR4拮抗剂Eritoran保护小鼠免受致命的流感感染

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随着流感病毒的继续演化以及它对现有抗病毒rn疗法抵抗力的不断蔓延,我们迫切需要新的抗rn流感疗法。以前的研究工作表明,TLR4信号rn作用介导小鼠由流感诱导的急性肺损伤、细胞rn因子生成和系统效应。现在,Stefarlie Voqelrn及其同事报告,Eritoran(一种合成TLR4拮抗rn剂)在被流感病毒感染之后长达6天施用,可保rn护小鼠不会死掉。现有抗病毒药物必须在感染rn后3天内施用才会有效。%There is a pressing need to develop alternatives to annual influenza vaccines and antiviral agents licensed for mitigating influenza infection. Previous studies reported that acute lung injury caused by chemical or microbial insults is secondary to the generation of host-derived, oxidized phospholipid that potently stimulates Toll-like receptor 4 (LR4)- dependent inflammation1. Subsequently, we reported that Tlr4-/-mice are highly refractory to influenza-induced lethality2, and proposed that therapeutic antagonism of TLR4 signalling would protect against influenza-induced acute lung injury.
机译:随着流感病毒的继续演化以及它对现有抗病毒rn疗法抵抗力的不断蔓延,我们迫切需要新的抗rn流感疗法。以前的研究工作表明,TLR4信号rn作用介导小鼠由流感诱导的急性肺损伤、细胞rn因子生成和系统效应。现在,Stefarlie Voqelrn及其同事报告,Eritoran(一种合成TLR4拮抗rn剂)在被流感病毒感染之后长达6天施用,可保rn护小鼠不会死掉。现有抗病毒药物必须在感染rn后3天内施用才会有效。%There is a pressing need to develop alternatives to annual influenza vaccines and antiviral agents licensed for mitigating influenza infection. Previous studies reported that acute lung injury caused by chemical or microbial insults is secondary to the generation of host-derived, oxidized phospholipid that potently stimulates Toll-like receptor 4 (LR4)- dependent inflammation1. Subsequently, we reported that Tlr4-/-mice are highly refractory to influenza-induced lethality2, and proposed that therapeutic antagonism of TLR4 signalling would protect against influenza-induced acute lung injury.

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  • 来源
    《Nature》 |2013年第7450期|498-502|共5页
  • 作者单位

    Department of Microbiology and Immunology, University of Maryland, Baltimore, Baltimore, Maryland 21201, USA;

    Department of Microbiology and Immunology, University of Maryland, Baltimore, Baltimore, Maryland 21201, USA;

    Department of Microbial Pathogenesis, University of Maryland, Baltimore, Baltimore,Maryland 21201,USA;

    Department of Pathology, University of Maryland, Baltimore, Baltimore, Maryland 21201, USA;

    Department of Microbiology and Immunology, University of Maryland, Baltimore, Baltimore, Maryland 21201, USA;

    Sigmovir Biosystems, Inc., Rockville, Maryland 20850, USA;

    Division of Molecular Immunology, Cincinnati Children's Hospital Research Foundation, Cincinnati, Ohio 45229, USA;

    Division of Molecular Immunology, Cincinnati Children's Hospital Research Foundation, Cincinnati, Ohio 45229, USA;

    The Inflammation Program, University of Iowa, Coralville, Iowa 52241, USA,Department of Veterans Affairs Medical Center, Iowa City, Iowa 52241, USA;

    Department of Veterans Affairs Medical Center, Iowa City, Iowa 52241, USA;

    Center for Vaccine Development, University of Maryland, Baltimore, Baltimore, Maryland 21201, USA;

    Department of Microbial Pathogenesis, University of Maryland, Baltimore, Baltimore,Maryland 21201,USA;

    Eisai, Inc.,Andover, Massachusetts 01810, USA;

    Eisai, Inc.,Andover, Massachusetts 01810, USA;

    Sigmovir Biosystems, Inc., Rockville, Maryland 20850, USA;

    Department of Microbiology and Immunology, University of Maryland, Baltimore, Baltimore, Maryland 21201, USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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  • 正文语种 eng
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  • 入库时间 2022-08-18 02:53:34

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