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Lipopolysaccharide-binding protein is required to combat a murine Gram-negative bacterial infection

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  • Robert S. Jack

    (Institut für Immunologie und Transfusionsmedizin, Ernst-Moritz-Arndt-Universität Greifswald)

  • Xiaolong Fan

    (Institut für Immunologie und Transfusionsmedizin, Ernst-Moritz-Arndt-Universität Greifswald)

  • Martin Bernheiden

    (Institut für Immunologie und Transfusionsmedizin, Ernst-Moritz-Arndt-Universität Greifswald)

  • Gabriele Rune

    (Institut für Anatomie, Ernst-Moritz-Arndt-Universität Greifswald)

  • Monika Ehlers

    (Institut für Immunologie und Transfusionsmedizin, Ernst-Moritz-Arndt-Universität Greifswald)

  • Albert Weber

    (Klinik und Polyklinik für Nuklearmedizin, Ernst-Moritz-Arndt-Universität Greifswald)

  • Gerhard Kirsch

    (Klinik und Polyklinik für Nuklearmedizin, Ernst-Moritz-Arndt-Universität Greifswald)

  • Renate Mentel

    (Institut für Medizinische Mikrobiologie, Ernst-Moritz-Arndt-Universität Greifswald)

  • Birgit Fürll

    (Institut für Immunologie und Transfusionsmedizin, Ernst-Moritz-Arndt-Universität Greifswald)

  • Marina Freudenberg

    (Max Planck Institut für Immunbiologie)

  • Gerd Schmitz

    (Universitätsklinikum, Klinische Chemie und Labormedizin)

  • Felix Stelter

    (Institut für Immunologie und Transfusionsmedizin, Ernst-Moritz-Arndt-Universität Greifswald)

  • Christine Schütt

    (Institut für Immunologie und Transfusionsmedizin, Ernst-Moritz-Arndt-Universität Greifswald)

Abstract

An invading pathogen must be held in check by the innate immune system until a specific immune response can be mounted. In the case of Gram-negative bacteria, the principal stimulator of the innate immune system is lipopolysaccharide (LPS), a component of the bacterial outer membrane1. In vitro, LPS is bound by lipopolysaccharide-binding protein (LBP)2 and transferred to CD14—the LPS receptor on the macrophage surface3,4—or to high-density lipoprotein (HDL) particles5,6. Transfer to CD14 triggers an inflammatory response which is crucial for keeping an infection under control. Here we investigate how LBP functions in vivo by using LBP-deficient mice. Surprisingly, we find that LBP is not required in vivo for the clearance of LPS from thecirculation, but is essential for the rapid induction of an inflammatory response by small amounts of LPS or Gram-negative bacteria and for survival of an intraperitoneal Salmonella infection.

Suggested Citation

  • Robert S. Jack & Xiaolong Fan & Martin Bernheiden & Gabriele Rune & Monika Ehlers & Albert Weber & Gerhard Kirsch & Renate Mentel & Birgit Fürll & Marina Freudenberg & Gerd Schmitz & Felix Stelter & C, 1997. "Lipopolysaccharide-binding protein is required to combat a murine Gram-negative bacterial infection," Nature, Nature, vol. 389(6652), pages 742-745, October.
    • Handle: RePEc:nat:nature:v:389:y:1997:i:6652:d:10.1038_39622
    DOI: 10.1038/39622
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    Cited by:

    1. Qilun Zhang & Xuting Shen & Xin Yuan & Jing Huang & Yaling Zhu & Tengteng Zhu & Tao Zhang & Haibo Wu & Qian Wu & Yinguang Fan & Jing Ni & Leilei Meng & Anyuan He & Chaowei Shi & Hao Li & Qingsong Hu &, 2024. "Lipopolysaccharide binding protein resists hepatic oxidative stress by regulating lipid droplet homeostasis," Nature Communications, Nature, vol. 15(1), pages 1-17, December.

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