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Related Experiment Videos

Complement component C5 modulates the systemic tumor necrosis factor response in murine endotoxic shock

P A Barton1, J S Warren

  • 1Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602.

Infection and Immunity
|April 1, 1993
PubMed
Summary

Complement component C5 significantly influences the body's response to endotoxins, impacting tumor necrosis factor (TNF) levels and disease severity in infections like meningococcemia. This highlights C5's crucial role in modulating inflammatory responses.

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Area of Science:

  • Immunology
  • Complement System
  • Inflammatory Response

Background:

  • Disseminated Neisseria meningitidis infections (meningococcemia) cause severe shock with high tumor necrosis factor (TNF) levels.
  • Individuals with deficiencies in late complement components (C5-C8) have increased neisserial infections but milder disease.
  • The role of terminal complement components (C5-C9) in modulating the systemic TNF response remains unclear.

Purpose of the Study:

  • To investigate the role of complement component C5 in modulating the systemic endotoxin-induced TNF response.
  • To compare the host response to lipopolysaccharide (LPS) in C5-deficient and complement-sufficient mice.

Main Methods:

  • Utilized C5-deficient (B10 D2/Osn) and complement-sufficient (B10 D2/Nsn) mice.
  • Administered lipopolysaccharide (LPS) to assess vascular permeability, illness severity, and serum TNF activity.

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  • Performed in vitro studies with macrophages and human monocytes using complement components and LPS.

    • Main Results:

    • Complement-sufficient mice showed increased vascular permeability, illness, and twofold higher serum TNF levels post-LPS compared to C5-deficient mice.
    • Reconstitution of C5-deficient mice with normal serum normalized vascular permeability and TNF levels.
    • In vitro, C5a induced TNF production in human monocytes, while C5b-C9 had no additional effect.

    Conclusions:

    • Complement component C5 plays a significant role in modulating the endotoxin-triggered TNF response.
    • C5 influences the severity of illness and vascular permeability during endotoxemia.
    • The function of complement components C5b-C9 in this specific response remains to be elucidated.