© 2001 by European Society of Cardiology
Copyright © 2001, European Society of Cardiology
Effects of interleukin-10 on monocyte/endothelial cell adhesion and MMP-9/TIMP-1 secretion
aU460 INSERM, X. Bichat School of Medicine, Paris, France
bImmunology Department and U479 INSERM, Bichat Hospital, Paris, France
cHassan II University, School of Sciences Ain chok, Department of Biology, Casablanca, Morocco
* Corresponding author. Tel.: +33-1-4485-6160; fax: +33-1-4485-6157 laurent.feldman{at}bch.ap-hop-paris.fr
Objective: Monocyte adhesion to endothelial cells and subsequent secretion of matrix metalloproteinases (MMPs) by activated macrophages are key events in arteriosclerosis and restenosis. We tested the hypothesis that interleukin-10 (IL-10), a potent anti-inflammatory cytokine, inhibits monocyte-endothelial cell interactions. Methods: The effect of IL-10 on monocyte/endothelial cell adhesion, as well as on the expression of MMP-9 and the tissue inhibitor of MMP-9, TIMP-1, were first tested in vitro in coculture systems. In addition, we used an ex vivo binding assay to study the inhibitory effect of IL-10 on monocyte adhesion to carotid arteries obtained from either normal, or L-nitro arginine-methyl ester (L-NAME)-treated rats. The effect of IL-10 on the expression of monocyte adhesion molecules (CD18 and CD62-L) was studied by flow cytometry. Results: IL-10 (150 ng/ml) inhibits monocyte adhesion to endothelial cells (by 35%) and to carotid arteries (by 40 and 50%, in normal and L-NAME-treated rats, respectively), via direct modulation of the expression of CD18 and CD62-L. Moreover, IL-10 dose-dependently decreases MMP-9 activity and increases TIMP-1 levels in coculture systems, both at the transcriptional level. Conclusions: Our results suggest that IL-10 is an important modulator of monocyte–endothelial cell interactions.
KEYWORDS Atherosclerosis; Cell culture/isolation; Cytokines; Leukocytes
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