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Mediators of Inflammation - Volume 12 2003, Issue 1, Pages 29-35

Immunology Division, Department of Pediatrics, Université de Sherbrooke, Sherbrooke J1H 5N4, QC, Canada



Copyright © 2003 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The objective of this study was to test the hypothesis that an oxidative stress can serve as a signal to regulate the expression of CCR5. When human monocytes were exposed to graded concentration of hydrogen peroxide H2O2, CCR5 mRNA levels increased maximally at 4 h of exposure to 200 μM of H2O2 and decreased by 24 h of treatment. Pretreatment of monocytes with the NF-κB inhibitor BAY 11-8072 blocked the H2O2-induced augmentation of CCR5 mRNA expression, suggesting a role for this transcription factor in the regulation of CCR5 expression. CCR5 protein expression on the plasma membrane was also increased by treatment with H2O2, as assessed by flow cytometry. This was accompanied by enhanced responsiveness of H2O2-pretreated monocytes to the CCR5 ligand MIP-1β in terms of chemotaxis and c-fos gene activation. Our results suggest that oxidative stress may indeed modulate the expression of chemokine receptors and thus contribute to regulation of the inflammatory process.





Autor: Geneviève Lehoux, Christian Le Gouill, Jana Stankova, and Marek Rola-pleszczynski

Fuente: https://www.hindawi.com/



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