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CCR5 is a receptor for Staphylococcus aureus leukotoxin ED

机译：CCR5是金黄色葡萄球菌白细胞毒素ED的受体

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摘要

金黄葡萄球菌表达优先杀死嗜中性细胞和其他rn免疫细胞的白细胞毒素。现在Victor Torres及rn其同事发现，白细胞毒素以表达趋化因子受体rnCCR5的细胞为目标，从而为这一免疫躲避机rn制的特异性提供了机制基础，同时也提出了可rn能的治疗目标。%Pore-forming toxins are critical virulence factors for many bacterial pathogens and are central to Staphylococcus aureus-mediated killing of host cells. S. aureus encodes pore-forming bi-component leukotoxins that are toxic towards neutrophils, but also specifically target other immune cells. Despite decades since the first description of staphylococcal leukocidal activity, the host factors responsible for the selectivity of leukotoxins towards different immune cells remain unknown. Here we identify the human immunodeficiency virus (HIV) co-receptor GCR5 as a cellular determinant required for cytotoxic targeting of subsets of myeloid cells and T lymphocytes by the S. aureus leukotoxin ED (LukED). We further demonstrate that LukED-dependent cell killing is blocked by CCR5 receptor antagonists, including the HIV drug maraviroc. Remarkably, CCR5-deficient mice are largely resistant to lethal S. aureus infection, highlighting the importance of CCR5 targeting in S. aureus pathogenesis. Thus, depletion of CCR5~+ leukocytes by LukED suggests a new immune evasion mechanism of S. aureus that can be therapeutically targeted.
机译：金黄葡萄球菌表达优先杀死嗜中性细胞和其他rn免疫细胞的白细胞毒素。现在Victor Torres及rn其同事发现，白细胞毒素以表达趋化因子受体rnCCR5的细胞为目标，从而为这一免疫躲避机rn制的特异性提供了机制基础，同时也提出了可rn能的治疗目标。%Pore-forming toxins are critical virulence factors for many bacterial pathogens and are central to Staphylococcus aureus-mediated killing of host cells. S. aureus encodes pore-forming bi-component leukotoxins that are toxic towards neutrophils, but also specifically target other immune cells. Despite decades since the first description of staphylococcal leukocidal activity, the host factors responsible for the selectivity of leukotoxins towards different immune cells remain unknown. Here we identify the human immunodeficiency virus (HIV) co-receptor GCR5 as a cellular determinant required for cytotoxic targeting of subsets of myeloid cells and T lymphocytes by the S. aureus leukotoxin ED (LukED). We further demonstrate that LukED-dependent cell killing is blocked by CCR5 receptor antagonists, including the HIV drug maraviroc. Remarkably, CCR5-deficient mice are largely resistant to lethal S. aureus infection, highlighting the importance of CCR5 targeting in S. aureus pathogenesis. Thus, depletion of CCR5~+ leukocytes by LukED suggests a new immune evasion mechanism of S. aureus that can be therapeutically targeted.

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  • 来源
    《Nature》 |2013年第7430期|51-55a3|共6页
  • 作者

    Francis Alonzo III; Lina Kozhaya; Stephen A. Rawlings; Tamara Reyes-Robles; Ashley L. DuMont; David G. Myszka; Nathaniel R. Landau; Derya Unutmaz; Victor J. Torres;

  • 作者单位

    Department of Microbiology, New York University School of Medicine, New York, New York 10016, USA;

    Department of Microbiology, New York University School of Medicine, New York, New York 10016, USA;

    Department of Microbiology, New York University School of Medicine, New York, New York 10016, USA;

    Department of Microbiology, New York University School of Medicine, New York, New York 10016, USA;

    Department of Microbiology, New York University School of Medicine, New York, New York 10016, USA;

    Biosensor Tools LLC, Salt Lake City, Utah 84103, USA;

    Department of Microbiology, New York University School of Medicine, New York, New York 10016, USA;

    Department of Microbiology, New York University School of Medicine, New York, New York 10016, USA,Department of Pathology, New York University School of Medicine, New York, New York 10016, USA,Department of Medicine, New York University School of Medicine, New York, New York 10016, USA;

    Department of Microbiology, New York University School of Medicine, New York, New York 10016, 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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