The effects of IgG and immune complexes on the endotoxin-induced cytokine response

S M Yentis1, R P Gooding, P G Riches

  • 1Department of Anaesthesia, Chelsea & Westminster Hospital, London, UK.

Cytokine
|May 1, 1994
PubMed

Insights

This study shows that endotoxin (LPS) and IgG immune complexes induce cytokines like IL-6, but the presence of complement activation and serum alters these responses, affecting IL-6 and TNF-alpha production.

Area of Science:

  • Immunology
  • Cellular Biology

Background:

  • Cytokine induction is crucial in immune responses.
  • Endotoxin (LPS) and IgG are key immune activators.
  • The role of complement and serum in modulating these responses requires further investigation.

Purpose of the Study:

  • To investigate cytokine induction (IL-1 beta, IL-6, TNF-alpha) in human whole blood stimulated by LPS and IgG.
  • To determine the influence of different media (plasma, serum, CSL) and complement activation on these inductions.
  • To analyze the effect of LPS/IgG immune complexes on cytokine profiles.

Main Methods:

  • Human peripheral whole blood cells were suspended in autologous plasma or serum diluted in basal medium or Compound Sodium Lactate Solution (CSL).
  • Cells were stimulated with LPS, IgG (Sandoglobulin), or preformed LPS/IgG immune complexes.
  • Cytokine levels (IL-1 beta, IL-6, TNF-alpha) and complement activation were measured.

Main Results:

  • LPS alone induced all three cytokines.
  • Sandoglobulin alone induced IL-6 in CSL-serum and TNF-alpha in plasma, with minimal IL-1 beta changes.
  • LPS/IgG immune complexes, in the presence of complement activation and/or serum, increased IL-1 beta and IL-6 while decreasing TNF-alpha, dissociating their production patterns.

Conclusions:

  • Complement activation and serum significantly modulate cytokine induction by LPS and IgG.
  • Sandoglobulin can induce IL-6 and suppress TNF-alpha under specific conditions (complement/serum presence).
  • Immune complex formation with LPS leads to a dissociation of IL-1 beta/IL-6 from TNF-alpha production when complement is activated.

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