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Platelet-activating factor contributes to Bacillus anthracis lethal toxin-associated damage.

Johanna Rivera1, Rani S Sellers2, Wangyong Zeng3

  • 1Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York 10461.

The Journal of Biological Chemistry
|January 31, 2014
PubMed
Summary
This summary is machine-generated.

Bacillus anthracis lethal toxin (LeTx) causes shock by increasing platelet-activating factor (PAF). Inhibiting PAF activity ameliorated LeTx-induced damage, suggesting PAF antagonists may treat anthrax shock.

Keywords:
Anthrax ToxinBacterial PathogenesisCytokineLipidsMacrophagesPlatelet-activating Factor

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Area of Science:

  • Pathology
  • Immunology
  • Microbiology

Background:

  • Lethal toxin (LeTx) from Bacillus anthracis is critical in anthrax shock pathogenesis.
  • Platelet-activating factor (PAF) is a lipid mediator involved in endotoxin-associated shock.

Purpose of the Study:

  • To investigate the role of PAF in the pathological effects of LeTx challenge in wild-type (WT) mice.

Main Methods:

  • WT mice were challenged with LeTx.
  • PAF activity was inhibited using PAF antagonists or PAF receptor-deficient mice were used.
  • Vascular permeability, hepatic necrosis, and cellular apoptosis were assessed.
  • Cytokine levels were measured.

Main Results:

  • LeTx challenge transiently increased serum PAF levels and decreased PAF acetylhydrolase activity.
  • PAF inhibition or absence of the PAF receptor ameliorated LeTx-induced vascular permeability changes, hepatic necrosis, and apoptosis.
  • PAF inhibition had minimal impact on cytokine levels.

Conclusions:

  • PAF significantly contributes to the pathology of LeTx-induced damage.
  • Targeting PAF may be a viable strategy for treating anthrax-associated shock.