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Related Experiment Video

Updated: Jul 11, 2026

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression
07:30

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression

Published on: June 15, 2019

Sepsis mediators.

François Philippart1, Jean-Marc Cavaillon

  • 1Unit Cytokines and Inflammation, Institut Pasteur, 28 rue Dr. Roux, 75015 Paris, France.

Current Infectious Disease Reports
|September 21, 2007
PubMed
Summary
This summary is machine-generated.

Sepsis elevates inflammatory markers, contributing to organ dysfunction and death. Counter-regulatory anti-inflammatory mediators can increase susceptibility to infections.

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Cecal Ligation Puncture Procedure
11:53

Cecal Ligation Puncture Procedure

Published on: May 7, 2011

Related Experiment Videos

Last Updated: Jul 11, 2026

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression
07:30

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression

Published on: June 15, 2019

Cecal Ligation Puncture Procedure
11:53

Cecal Ligation Puncture Procedure

Published on: May 7, 2011

Area of Science:

  • Immunology
  • Pathophysiology
  • Biochemistry

Background:

  • Sepsis is characterized by elevated plasma inflammatory markers.
  • These mediators contribute to sepsis-induced organ dysfunction and mortality.
  • Experimental models confirm the role of specific mediators in sepsis pathology.

Purpose of the Study:

  • To review the role of inflammatory mediators in sepsis.
  • To discuss the contribution of various mediators to sepsis pathogenesis.
  • To highlight the impact of anti-inflammatory mediators on host immunity.

Main Methods:

  • Review of experimental models using transgenic/gene-targeted animals.
  • Analysis of studies using neutralizing agents against specific mediators.
  • Examination of data on anaphylatoxins, coagulation/fibrinolysis factors, cytokines, chemokines, proteases, lipid mediators, nitric oxide, and high mobility group box-1.

Main Results:

  • Anaphylatoxins, coagulation factors, cytokines, chemokines, proteases, lipid mediators, nitric oxide, and high mobility group box-1 contribute to sepsis-related organ damage.
  • The activation of the complement system generates anaphylatoxins, exacerbating sepsis.
  • Counter-regulatory anti-inflammatory cytokines and neuromediators can impair host immunity.

Conclusions:

  • Multiple inflammatory mediators play critical roles in the pathophysiology of sepsis.
  • Understanding these mediators is crucial for developing therapeutic strategies.
  • Impaired host immunity due to anti-inflammatory responses increases vulnerability to secondary infections.