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AhR sensing of bacterial pigments regulates antibacterial defence

机译：AhR感测细菌色素可调节抗菌防御

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摘要

The aryl hydrocarbon receptor (AhR) is a highly conserved ligand-dependent transcription factor that senses environmental toxins and endogenous ligands, thereby inducing detoxifying enzymes and modulating immune cell differentiation and responses. We hypothesized that AhR evolved to sense not only environmental pollutants but also microbial insults. We characterized bacterial pigmented virulence factors, namely the phenazines from Pseudomonas aeruginosa and the naphthoquinone phthiocol from Mycobacterium tuberculosis, as ligands of AhR. Upon ligand binding, AhR activation leads to virulence factor degradation and regulated cytokine and chemokine production. The relevance of AhR to host defence is underlined by heightened susceptibility of AhR-deficient mice to both P. aeruginosa and M. tuberculosis. Thus, we demonstrate that AhR senses distinct bacterial virulence factors and controls antibacterial responses, supporting a previously unidentified role for AhR as an intracellular pattern recognition receptor, and identify bacterial pigments as a new class of pathogen-associated molecular patterns.%这篇论文显示, 芳烃受体(AhR, 已知能识别环境毒素、自身分子和饮食成分）也是针对细菌的先天防卫系统的一个组成部分, 充当来自肺病原体的有色毒力因子的一个直接传感器。细菌配体与AhR的结合, 会通过一个负反馈环促进它们降解, 同时促进细胞因子和趋化因子的生成。AhR不足的小鼠对绿脓杆菌和结核杆菌都高度敏感。
机译：芳烃受体（AhR）是高度保守的依赖配体的转录因子，可感应环境毒素和内源性配体，从而诱导解毒酶并调节免疫细胞的分化和反应。我们假设，AhR不仅可以感知环境污染物，还可以感知微生物污染。我们表征细菌色素的毒力因子，即铜绿假单胞菌的吩嗪和结核分枝杆菌的萘醌苯硫酚，作为AhR的配体。配体结合后，AhR激活会导致毒力因子降解并调节细胞因子和趋化因子的产生。缺乏AhR的小鼠对铜绿假单胞菌和结核分枝杆菌的敏感性都增强了AhR与宿主防御的相关性。因此，我们证明了AhR可以感知不同的细菌毒力因子并控制抗菌反应，支持AhR作为细胞内模式识别受体的先前未确定的作用，并将细菌色素识别为与病原体相关的新型分子模式。 ，芳烃受体（AhR，已知能识别环境毒素，自身分子和饮食成分也是针对细菌的先天防卫系统的一个组成部分，可以从肺病原体的有色毒力因子的一个直接传感器。细菌配体与AhR的结合，会通过一个负反馈环促进它们降解，同时促进细胞因子和趋化因子的生成。AhR不足的小鼠对绿脓杆菌和结核杆菌高度高度敏感。

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  • 来源
    《Nature》 |2014年第7515期|387-392337|共7页
  • 作者

    Pedro Moura-Alves; Kellen Fae; Erica Houthuys; Anca Dorhoi; Annika Kreuchwig; Jens Furkert; Nicola Barison; Anne Diehl; Antje Munder; Patricia Constant; Tatsiana Skrahina; Ute Guhlich-Bornhof; Marion Klemm; Anne-Britta Koehler; Silke Bandermann; Christian Goosmann; Hans-Joachim Mollenkopf; Robert Hurwitz; Volker Brinkmann; Simon Fillatreau; Mamadou Daffe; Burkhard Tuemmler; Michael Kolbe; Hartmut Oschkinat; Gerd Krause; Stefan H. E. Kaufmann;

  • 作者单位

    Max Planck Institute for Infection Biology, Department of Immunology, Chariteplatz 1, 10117 Berlin, Germany;

    Max Planck Institute for Infection Biology, Department of Immunology, Chariteplatz 1, 10117 Berlin, Germany;

    Max Planck Institute for Infection Biology, Department of Immunology, Chariteplatz 1, 10117 Berlin, Germany;

    Max Planck Institute for Infection Biology, Department of Immunology, Chariteplatz 1, 10117 Berlin, Germany;

    Leibniz Institute for Molecular Pharmacology (FMP), Robert-Roessle-Strasse 10, 13125 Berlin, Germany;

    Leibniz Institute for Molecular Pharmacology (FMP), Robert-Roessle-Strasse 10, 13125 Berlin, Germany;

    Max Planck Institute for Infection Biology, Structural Systems Biology, Chariteplatz 1, 10117 Berlin, Germany;

    Leibniz Institute for Molecular Pharmacology (FMP), Robert-Roessle-Strasse 10, 13125 Berlin, Germany;

    Clinical Research Group, Clinic for Pediatric Pneumology, Allergology and Neonatology, OE 6710, Hannover Medical School, Carl-Neuberg-Str. 1, 30625 Hannover, Germany;

    Institute of Pharmacology and Structural Biology (IPBS), CNRS and University of Toulouse (Toulouse Ⅲ), 205 Route de Narbonne, 31077, Toulouse cedex 04, Toulouse, France;

    Max Planck Institute for Infection Biology, Department of Immunology, Chariteplatz 1, 10117 Berlin, Germany;

    Max Planck Institute for Infection Biology, Department of Immunology, Chariteplatz 1, 10117 Berlin, Germany;

    Max Planck Institute for Infection Biology, Department of Immunology, Chariteplatz 1, 10117 Berlin, Germany;

    Max Planck Institute for Infection Biology, Department of Immunology, Chariteplatz 1, 10117 Berlin, Germany;

    Max Planck Institute for Infection Biology, Department of Immunology, Chariteplatz 1, 10117 Berlin, Germany;

    Microscopy Core Facility, Max Planck Institute for Infection Biology, Department of Immunology, Chariteplatz 1, 10117 Berlin, Germany;

    Microarray Core Facility, Max Planck Institute for Infection Biology, Departmentof Immunology, Chariteplatz 1, 10117 Berlin, Germany;

    Protein Purification Core Facility, Max Planck Institute for infection Biology, Chariteplatz 1, 10117 Berlin, Germany;

    Microscopy Core Facility, Max Planck Institute for Infection Biology, Department of Immunology, Chariteplatz 1, 10117 Berlin, Germany;

    German Rheumatism Research Centre Berlin (DRFZ), a Leibniz Institute, Chariteplatz 1, 10117 Berlin, Germany;

    Institute of Pharmacology and Structural Biology (IPBS), CNRS and University of Toulouse (Toulouse Ⅲ), 205 Route de Narbonne, 31077, Toulouse cedex 04, Toulouse, France;

    Clinical Research Group, Clinic for Pediatric Pneumology, Allergology and Neonatology, OE 6710, Hannover Medical School, Carl-Neuberg-Str. 1, 30625 Hannover, Germany;

    Max Planck Institute for Infection Biology, Structural Systems Biology, Chariteplatz 1, 10117 Berlin, Germany;

    Leibniz Institute for Molecular Pharmacology (FMP), Robert-Roessle-Strasse 10, 13125 Berlin, Germany;

    Leibniz Institute for Molecular Pharmacology (FMP), Robert-Roessle-Strasse 10, 13125 Berlin, Germany;

    Max Planck Institute for Infection Biology, Department of Immunology, Chariteplatz 1, 10117 Berlin, Germany;

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