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Association of serum tumor necrosis factor levels with decrease of cholesterol during septic shock

P Fraunberger1, G Pilz, P Cremer

  • 1Department of Clinical Chemistry, University Hospital, Grosshadern, Munich, Germany.

Shock (Augusta, Ga.)
|December 5, 1998
PubMed
Summary
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Tumor necrosis factor alpha (TNF) causes hypocholesterolemia during septic shock by increasing low-density lipoprotein degradation. High TNF levels in sepsis significantly lower cholesterol, even with elevated TNF receptors.

Area of Science:

  • Biochemistry
  • Immunology
  • Pathophysiology

Background:

  • Inflammatory conditions like septic shock are linked to decreased cholesterol levels (hypocholesterolemia).
  • Tumor necrosis factor alpha (TNF) is a key cytokine implicated in inflammatory diseases.

Purpose of the Study:

  • To investigate if TNF directly causes hypocholesterolemia.
  • To assess the relationship between TNF levels, cholesterol, and related lipoproteins in septic shock patients.

Main Methods:

  • Measured serum levels of TNF, TNF receptors (p55 and p75), total cholesterol, Apo A1, and Apo B in septic shock patients over 8 days.
  • Conducted in vitro studies using cultured cells (fibroblasts, endothelial cells, HepG2) to examine TNF's effect on low-density lipoprotein (LDL) degradation.
  • Assessed the impact of recombinant soluble TNF receptors on TNF-induced LDL receptor activity.

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Main Results:

  • Septic shock patients exhibited significantly higher serum TNF and TNF receptor levels compared to healthy controls.
  • Increased cytokine levels correlated with a significant decline in serum total cholesterol, Apo A1, and Apo B.
  • In vitro, TNF increased LDL degradation in all tested cell lines; recombinant TNF receptors partially inhibited this effect, but were less effective in patient serum ratios.

Conclusions:

  • Serum TNF levels are a primary determinant of hypocholesterolemia in sepsis and septic shock.
  • Despite the presence of TNF receptors, elevated TNF drives cholesterol reduction.
  • TNF plays a confirmed role in the development of hypocholesterolemia during inflammatory states.