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Blood, 1 May 2005, Vol. 105, No. 9, pp. 3413-3419.
Prepublished online as a Blood First Edition Paper on January 11, 2005; DOI 10.1182/blood-2004-10-4111.
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Submitted October 26, 2004
Accepted December 19, 2004
TRAIL counteracts the pro-adhesive activity of inflammatory cytokines in endothelial cells by down-modulating CCL8 and CXCL10 chemokine expression and release
Paola Secchiero*, Federica Corallini, Maria G di Iasio, Arianna Gonelli, Elisa Barbarotto, and Giorgio Zauli
Department of Morphology and Embryology, Human Anatomy Section, University of Ferrara, Ferrara, Italy
Department of Normal Human Morphology, University of Trieste, Trieste, Italy
* Corresponding author; email: secchier{at}mail.umbi.umd.edu.
Exposure of endothelial cells to recombinant TNF-related apoptosis inducing ligand (TRAIL) induced a modest (two-fold) increase of HL-60 cell adhesion, as compared to TNF- (forty-fold) or IL-1 (twenty-fold). However, pretreatment of endothelial cultures with TRAIL determined a significant reduction of the pro-adhesive activity induced by both TNF- and IL-1. Unexpectedly, the anti-adhesive activity of TRAIL was not due to interference with the NF-kB-mediated upregulation of surface ICAM-1, VCAM-1 and E-selectin adhesion molecules in response to inflammatory cytokines. In searching for the molecular mechanism underlying this biological activity of TRAIL, a cDNA microarray analysis was performed. TRAIL pre-treatment variably down-modulated the mRNA steady-state levels of several TNF--induced chemokines, and, in particular, it abrogated the TNF--mediated up-regulation of CCL8 and CXCL10. Of note, the addition of optimal concentrations of recombinant CCL8 plus CXCL10 to endothelial cultures completely restored the pro-adhesive activity of TNF-. Moreover, experiments performed with agonistic anti-TRAIL-receptor antibodies demonstrated that both TRAIL-R1 and TRAIL-R2 contributed, although at different levels, to TRAIL-induced chemokine modulation. Taken together, our data suggest that TRAIL might play an important role in modulating leukocyte/endothelial cell adhesion, by selectively down-regulating CCL8 and CXCL10 chemokines.
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