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Related Experiment Video

Updated: May 17, 2026

A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats

A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats

Published on: February 20, 2021

The role of complement system in septic shock.

Jean Charchaflieh¹, Jiandong Wei, Georges Labaze

¹Department of Anesthesiology, SUNY Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, NY 11203, USA.

Clinical & Developmental Immunology

|October 11, 2012

Summary

Septic shock involves complement system activation. Early decreases in mannose-binding lectin-associated serine protease-2 (MASP-2) may predict mortality in septic shock patients.

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

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Published on: June 15, 2019

Area of Science:

Immunology
Critical Care Medicine
Biochemistry

Background:

Septic shock is a life-threatening condition with high mortality.
Complement system activation, particularly C3 and C5, is implicated in septic shock pathogenesis.
The roles of the classical, alternative, and lectin complement pathways in septic shock are complex and require further elucidation.

Purpose of the Study:

To explore the intricate involvement of the three upstream complement pathways in septic shock.
To investigate the potential protective role of mannose-binding lectin (MBL) in sepsis.
To analyze the correlation between MBL-associated serine protease-2 (MASP-2) levels and mortality in septic shock patients.

Main Methods:

Review of basic and clinical studies on complement activation in septic shock.
Analysis of preliminary data from septic shock patients regarding MASP-2 levels.
Discussion of pathogenic mechanisms and potential therapeutic interventions related to complement activation.

Main Results:

Both classical and alternative complement pathways are activated in septic shock, with the alternative pathway potentially activating earlier.
The lectin pathway, specifically MBL, may have a protective role against sepsis.
A preliminary finding suggests that an acute decrease in MASP-2 in the early phase of septic shock correlates with in-hospital mortality.

Conclusions:

The precise contribution of excessive activation of the three upstream complement pathways to septic shock's detrimental effects remains to be fully determined.
MASP-2 levels may serve as a potential early biomarker for mortality risk in septic shock.
Further research into complement-related mechanisms and therapeutic strategies is crucial for improving septic shock outcomes.