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Updated: Aug 12, 2026

Intravenous Endotoxin Challenge in Healthy Humans: An Experimental Platform to Investigate and Modulate Systemic Inflammation
07:48

Intravenous Endotoxin Challenge in Healthy Humans: An Experimental Platform to Investigate and Modulate Systemic Inflammation

Published on: May 16, 2016

Role of endotoxin in mononuclear phagocyte-mediated inflammatory responses

R W Watson1, H P Redmond, D Bouchier-Hayes

  • 1Department of Surgery, RCSI, Beaumont Hospital, Dublin, Ireland.

Journal of Leukocyte Biology
|July 1, 1994
PubMed

Insights

Lipopolysaccharide (LPS) from bacteria triggers septic shock by activating immune cells like mononuclear phagocytes (MP). This review examines LPS-MP interactions and potential therapies to inhibit them.

Area of Science:

  • Immunology
  • Pathogenesis
  • Bacteriology

Background:

  • Lipopolysaccharide (LPS) is a key component of gram-negative bacteria cell walls.
  • LPS initiates septic shock by activating immune cells, particularly mononuclear phagocytes (MP).
  • MP bind LPS via the CD14 receptor, releasing inflammatory mediators.

Purpose of the Study:

  • To review the mechanisms of LPS-MP interaction.
  • To explore therapeutic strategies targeting LPS-MP interaction.
  • To understand the role of LPS in septic shock pathogenesis.

Main Methods:

  • Literature review of LPS-immune cell interactions.
  • Analysis of CD14 receptor-mediated signaling pathways.
  • Evaluation of existing and potential therapeutic interventions.

Main Results:

  • LPS-MP interaction is central to the inflammatory response in sepsis.
  • CD14 receptor is crucial for LPS recognition by MP.
  • Therapeutic inhibition of LPS-MP interaction shows promise.

Conclusions:

  • Understanding LPS-MP interaction is vital for managing septic shock.
  • Targeting the CD14 pathway offers a potential therapeutic avenue.
  • Further research is needed to develop effective anti-LPS therapies.

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