AI Article Synopsis
- The lethal toxin (LeTx) from Bacillus anthracis is a key factor in causing shock during anthrax infections, while platelet-activating factor (PAF) is linked to shock from endotoxins.
- In experiments with wild-type mice, LeTx exposure led to increased PAF levels and reduced PAF acetylhydrolase activity, suggesting a role for PAF in toxic responses.
- Using PAF antagonists or testing PAF receptor-negative mice helped reduce symptoms like vascular damage and liver cell death from LeTx, indicating that PAF antagonists could be useful in treating anthrax-related shock.
Article Abstract
The lethal toxin (LeTx) of Bacillus anthracis plays a central role in the pathogenesis of anthrax-associated shock. Platelet-activating factor (PAF) is a potent lipid mediator that has been implicated in endotoxin-associated shock. In this study, we examined the contribution of PAF to the manifestations of lethal toxin challenge in WT mice. LeTx challenge resulted in transient increase in serum PAF levels and a concurrent decrease in PAF acetylhydrolase activity. Inhibition of PAF activity using PAF antagonists or toxin challenge of PAF receptor negative mice reversed or ameliorated many of the pathologic features of LeTx-induced damage, including changes in vascular permeability, hepatic necrosis, and cellular apoptosis. In contrast, PAF inhibition had minimal effects on cytokine levels. Findings from these studies support the continued study of PAF antagonists as potential adjunctive agents in the treatment of anthrax-associated shock.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3945373 | PMC |
| http://dx.doi.org/10.1074/jbc.M113.524900 | DOI Listing |
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