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Related Experiment Videos

Circulating concentrations of adiponectin, an endogenous lipopolysaccharide neutralizing protein, decrease in rats

Hiroshi Tsuchihashi1, Hiroshi Yamamoto, Kazuhisa Maeda

  • 1Department of Surgery, Shiga University of Medical Science, Shiga, Japan.

The Journal of Surgical Research
|February 21, 2006
PubMed
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Adiponectin neutralizes lipopolysaccharide (LPS) in vitro, reducing its inflammatory activity. In sepsis models, adiponectin levels decrease as LPS and TNF-alpha increase, suggesting adiponectin

Area of Science:

  • Endocrinology
  • Immunology
  • Biochemistry

Background:

  • Adiponectin, an anti-inflammatory cytokine produced by adipocytes, has an incompletely understood interaction with lipopolysaccharide (LPS).
  • Investigating adiponectin's effects on LPS is crucial for understanding inflammatory responses.

Purpose of the Study:

  • To elucidate the interaction between adiponectin and lipopolysaccharide (LPS).
  • To determine the effect of adiponectin on LPS activity in vitro and in a polymicrobial sepsis model.

Main Methods:

  • In vitro incubation of recombinant adiponectin with LPS, followed by Limulus amoebocyte lysate (LAL) assay and Western blotting.
  • Induction of polymicrobial sepsis in rodents via cecal ligation and puncture (CLP) to measure plasma adiponectin, endotoxin, and tumor necrosis factor-alpha (TNF-alpha) levels.

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Main Results:

  • Adiponectin dose-dependently suppressed LAL activity, indicating neutralization of LPS.
  • Western blotting showed a mass shift when adiponectin interacted with LPS.
  • In CLP-induced sepsis, plasma adiponectin levels decreased significantly, while endotoxin and TNF-alpha levels increased.
  • Plasma adiponectin levels negatively correlated with plasma endotoxin levels.

Conclusions:

  • Adiponectin demonstrates in vitro neutralization of LPS, diminishing its activity.
  • Adiponectin's anti-inflammatory effects in sepsis may be partly attributed to LPS neutralization.
  • Adiponectin plays a role in modulating the inflammatory response to LPS during sepsis.