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Related Experiment Videos

P-selectin binds to bacterial lipopolysaccharide

R Malhotra1, R Priest, M R Foster

  • 1Glycobiology Research Unit, Glaxo-Wellcome Medicines Research Centre, Stevenage, GB. RM18326@ggr.co.uk

European Journal of Immunology
|April 29, 1998
PubMed
Summary

P-selectin acts as a receptor for lipopolysaccharide (LPS) on platelets, contributing to organ failure in septic shock. This finding reveals a key interaction in the disease

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Area of Science:

  • Immunology
  • Hematology
  • Pathophysiology

Background:

  • Septic shock frequently leads to multiple organ failure, often involving disseminated intravascular coagulation.
  • Lipopolysaccharide (LPS)-induced organ failure is linked to platelet and neutrophil accumulation in organs.
  • The platelet surface receptor for LPS is currently unknown, hindering understanding of LPS-platelet interactions.

Purpose of the Study:

  • To identify the specific surface receptor responsible for lipopolysaccharide (LPS) binding on platelets.
  • To elucidate the role of this receptor in the context of LPS-induced organ failure in septic shock.

Main Methods:

  • Investigated the interaction between LPS and platelets using fluorescein isothiocyanate (FITC)-conjugated LPS.
  • Utilized P-selectin as a potential LPS receptor, testing binding in the presence of anti-P-selectin antibodies, lipid A, and fucoidan.

Related Experiment Videos

  • Compared LPS binding on thrombin-activated versus untreated platelets.

    • Main Results:

    • P-selectin was identified as a functional receptor for LPS on platelets.
    • LPS binding to P-selectin was independent of calcium ions (Ca2+).
    • Binding was inhibited by anti-P-selectin antibodies, lipid A, and fucoidan, with significantly increased LPS binding on activated platelets.

    Conclusions:

    • P-selectin mediates the binding of LPS to platelets.
    • This LPS-P-selectin interaction, particularly on activated platelets or epithelium, likely plays a significant role in the pathophysiology of organ failure during septic shock.
    • Identifying this receptor offers potential therapeutic targets for septic shock complications.