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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Mast cells elicit proinflammatory but not type I interferon responses upon activation of TLRs by bacteria
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Mast cells elicit proinflammatory but not type I interferon responses upon activation of TLRs by bacteria

机译：肥大细胞在细菌激活TLR时引发促炎反应，但不引起I型干扰素反应

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摘要

Balanced induction of proinflammatory and type I IFN responses upon activation of Toll-like receptors (TLRs) determines the outcome of microbial infections and the pathogenesis of autoimmune and other inflammatory diseases. Mast cells, key components of the innate immune system, are known for their debilitating role in allergy and autoimmunity. However, their role in antimicrobial host defenses is being acknowledged increasingly. How mast cells interact with microbes and the nature of responses triggered thereby is not well characterized. Here we show that in response to TLR activation by Gram-positive and -negative bacteria or their components, mast cells elicit proinflammatory but not type I IFN responses. We demonstrate that in mast cells, bound bacteria and TLR ligands remain trapped at the cell surface and do not undergo internalization, a prerequisite for type I IFN induction. Such cells, however, can elicit type I IFNs in response to vesicular stomatitis virus which accesses the cytosolic retinoic acid-inducible gene I receptor. Although important for antiviral immunity, a strong I IFN response is known to contribute to pathogenesis of several bacterial pathogens such as Listeria monocytogenes. Interestingly, we observed that the mast cell-dependent neutrophil mobilization upon L. monocytogenes infection is highly impaired by IFN-β. Thus, the fact that mast cells, although endowed with the capacity to elicit type I IFNs in response to viral infection, elicit only proinflammatory responses upon bacterial infection shows that mast cells, key effector cells of the innate immune system, are well adjusted for optimal antibacterial and antiviral responses.
机译：Toll样受体（TLR）激活后促炎和I型IFN反应的均衡诱导决定了微生物感染的结果以及自身免疫性疾病和其他炎性疾病的发病机理。肥大细胞是先天免疫系统的关键组成部分，以其在变态反应和自身免疫中的虚弱作用而闻名。但是，它们在抗微生物宿主防御中的作用越来越得到认可。肥大细胞如何与微生物相互作用以及由此触发的反应的性质尚未得到很好的表征。在这里，我们显示了对革兰氏阳性和阴性细菌或其成分对TLR激活的响应，肥大细胞引起促炎性反应，而不引起I型IFN反应。我们证明，在肥大细胞中，结合的细菌和TLR配体仍然被困在细胞表面并且不经历内化作用，这是I型IFN诱导的前提。然而，此类细胞可响应水泡性口炎病毒（访问胞质视黄酸诱导型基因I受体）而诱发I型干扰素。尽管对抗病毒免疫很重要，但已知强烈的I IFN应答可导致多种细菌性病原体（如单核细胞增生性李斯特菌）的发病。有趣的是，我们观察到单核细胞增生李斯特氏菌感染后肥大细胞依赖的嗜中性白细胞动员受到IFN-β的极大损害。因此，尽管肥大细胞具有响应病毒感染引起I型IFN的能力，但仅在细菌感染时才引起促炎反应，这一事实表明，肥大细胞（先天免疫系统的关键效应细胞）已被很好地调节以达到最佳抗菌和抗病毒反应。

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  • 作者

    Nicole Dietrich; Manfred Rohde; Robert Geffers; Andrea Kroeger; Hansjoerg Hauser; Siegfried Weiss; Nelson O. Gekara;

  • 作者单位

    Departments of Molecular Immunology, Helmholtz-Centre for Infection Research, 38124 Braunschweig, Germany;

    Departments of Microbial Pathogenesis, Helmholtz-Centre for Infection Research, 38124 Braunschweig, Germany;

    Departments of Cell Biology, Helmholtz-Centre for Infection Research, 38124 Braunschweig, Germany;

    Gene Regulation and Differentiation, Helmholtz-Centre for Infection Research, 38124 Braunschweig, Germany;

    Gene Regulation and Differentiation, Helmholtz-Centre for Infection Research, 38124 Braunschweig, Germany;

    Departments of Molecular Immunology, Helmholtz-Centre for Infection Research, 38124 Braunschweig, Germany;

    Departments of Molecular Immunology, Helmholtz-Centre for Infection Research, 38124 Braunschweig, Germany Institute for Genetics, University of Cologne, 50674 Cologne, Germany;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    endolysosome; innate immunity; listeria; salmonella; vesicular stomatitis virus;

    机译：溶酶体先天免疫;李斯特菌;沙门氏菌;水泡性口炎病毒;

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