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Endogenous antimicrobial peptide LL-37 induces human vasodilatation
I Berkestedt1, A Nelson, M Bodelsson
1Section of Anaesthesiology and Intensive Care, Department of Clinical Sciences, Lund University, SE-221 85 Lund, Sweden.
British Journal of Anaesthesia
|April 10, 2008
Summary
The antimicrobial peptide LL-37 causes blood vessels to relax by acting on the ALX receptor in veins. This finding suggests potential new treatments for septic shock involving ALX antagonists.
Area of Science:
- Vascular biology
- Immunology
- Pharmacology
Background:
- Septic shock involves vasodilation and innate immune activation, releasing antimicrobial peptides like LL-37.
- LL-37 attracts leukocytes via the lipoxin A(4) receptor (ALX), which is also found in vascular endothelial cells.
Purpose of the Study:
- To investigate the effect of LL-37 on vascular tone for potential pharmacological intervention in septic shock.
Main Methods:
- Human omental arteries and veins were studied for smooth muscle activity in organ baths.
- Gene expression was analyzed using reverse transcriptase-polymerase chain reaction.
Main Results:
- LL-37 induced endothelium-dependent relaxation in veins, but not arteries, at micromolar concentrations.
- This relaxation was mediated via the ALX receptor and involved nitric oxide and EDHF, but not prostanoids.
- ALX expression was confirmed in the vein endothelium.
Conclusions:
- The antimicrobial peptide LL-37 induces endothelium-dependent relaxation in human omental veins through endothelial ALX.
- LL-37 may contribute to vasodilation in sepsis, and ALX antagonists could be a potential therapeutic strategy.
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