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PR-39, a proline/arginine-rich antimicrobial peptide, prevents postischemic microvascular dysfunction.

R J Korthuis1, D C Gute, F Blecha

  • 1Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, School of Medicine in Shreveport, Shreveport, Louisiana 71130, USA. rkorth@lsumc.edu

The American Journal of Physiology
|September 14, 1999
PubMed
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PR-39, a neutrophil antibacterial peptide, prevents intestinal ischemia-reperfusion injury by inhibiting leukocyte adhesion and oxidant production. This peptide may offer therapeutic benefits for postischemic inflammation.

Area of Science:

  • Biomedical Science
  • Physiology
  • Immunology

Background:

  • Intestinal ischemia-reperfusion (I/R) injury increases oxidant production, disrupting the microvascular barrier.
  • Activated neutrophils contribute significantly to tissue damage during reperfusion.

Purpose of the Study:

  • To investigate if PR-39, a neutrophil NADPH oxidase inhibitor, prevents postischemic oxidant production and microvascular leakage.
  • To evaluate PR-39's effect on leukocyte adhesion and emigration during I/R.

Main Methods:

  • In vivo studies monitored oxidant production, protein leakage, and leukocyte activity in rat mesenteric venules subjected to I/R with or without PR-39.
  • In vitro experiments assessed PR-39's impact on neutrophil chemotaxis and endothelial cell adhesion molecule expression.

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Main Results:

  • PR-39 administration abolished I/R-induced leukocyte adhesion and emigration.
  • PR-39 inhibited oxidant production and venular protein leakage during reperfusion.
  • In vitro, PR-39 reduced neutrophil chemotaxis and endothelial cell adhesion molecule-1 expression.

Conclusions:

  • PR-39 effectively prevents postischemic leukocyte adhesion and emigration.
  • PR-39's anti-inflammatory effects are likely mediated by its antiadhesive properties.
  • PR-39 shows therapeutic potential for mitigating neutrophil-driven inflammation in I/R injury.