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

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 and Christine Schütt
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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

Nature, 1997, vol. 389, issue 6652, 742-745

Abstract: 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.

Date: 1997
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DOI: 10.1038/39622

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