Genre
- Journal Article
The porcine antimicrobial peptide, PR-39, has several activities beyond its function of killing bacteria. Here we report that PR-39 alters macrophage viability by inhibiting apoptosis, which was induced by nutrient depletion, LPS stimulation or camptothecin treatment. This antiapoptotic effect was pronounced resulting in significant reductions in annexin-V binding to externalized phosphatidylserine and was associated with a decrease in caspase-3 activity. These findings suggest that PR-39, a porcine neutrophil-derived antimicrobial peptide, might function in the inflammatory milieu not only to kill bacteria, but also to aid in modulating the viability of inflammatory cells by regulating apoptosis.
Department of Anatomy and Physiology, College of Veterinary Medicine, Kansas State University, Coles Hall 228, 1600 Denison Avenue, Manhattan, KS 66506-5602, USA.
United States
LR: 20061115; PUBM: Print; JID: 7708205; 0 (Annexin A5); 0 (Antimicrobial Cationic Peptides); 0 (Enzyme Inhibitors); 0 (Lipopolysaccharides); 139637-11-9 (PR 39); 7689-03-4 (Camptothecin); EC 3.4.22.- (Casp3 protein, mouse); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspases); ppublish
Source type: Electronic(1)
Language
- English
Subjects
- Antimicrobial Cationic Peptides/pharmacology
- animals
- Cells, Cultured
- Mice
- Lipopolysaccharides/pharmacology
- DNA Fragmentation/drug effects
- Enzyme Inhibitors/pharmacology
- Macrophages/drug effects/metabolism
- Caspase 3
- Apoptosis/drug effects
- Caspases/metabolism
- Annexin A5/metabolism
- Camptothecin/pharmacology
- Swine