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J. Biol. Chem., Vol. 276, Issue 28, 26051-26056, July 13, 2001
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From the Extracellular nucleotides are autocrine and
paracrine cellular mediators that signal through P2 nucleotide
receptors. Monocytic cells express several P2Y receptors but the role
of these G protein-coupled receptors in monocytes is not known. Here,
we present evidence that P2Y6 regulates chemokine
production and release in monocytes. We find that UDP, a selective
P2Y6 agonist, stimulates interleukin (IL)-8 release
in human THP-1 monocytic cells whereas other nucleotides are relatively
inactive. P2 receptor antagonists or P2Y6 antisense oligonucleotides inhibit IL-8 release induced by UDP. Furthermore, UDP
specifically activated IL-8 production in astrocytoma 1321N1 cells
transfected with human P2Y6. Since lipopolysaccharide has been suggested to activate P2 receptors via nucleotide release, we
tested whether IL-8 production stimulated by lipopolysaccharide might
result from P2Y6 activation. P2 antagonists or apyrase, an
enzyme which hydrolyzes nucleotides including UDP, inhibit IL-8
production induced by lipopolysaccharide but not by other stimuli.
Furthermore, IL-8 gene expression activated by lipopolysaccharide is
enhanced by P2Y6 overexpression and inhibited by
P2Y6 antisense oligonucleotides. Thus, UDP activates IL-8
production via P2Y6 in monocytic cells. Furthermore,
lipopolysaccharide mediates IL-8 production at least in part by
autocrine P2Y6 activation. These findings indicate a novel
role for P2Y6 in innate immune defenses.
P2Y6 Nucleotide Receptor Mediates Monocyte
Interleukin-8 Production in Response to UDP or
Lipopolysaccharide*
§,,,,
, and
Gastroenterology Divison and Signal
Transduction Division, Beth Israel Deaconess Medical Center, Harvard
Medical School, Boston, Massachusetts 02215 and the ¶ Institute of
Interdisciplinary Research, Medical School, Université Libre de
Bruxelles, Route de Lennik 808, 1070 Brussels, Belgium
*
This work was supported by a Fellowship Award from the
Crohn's and Colitis Foundation of America (to M. W.), National
Institutes of Health Grants RO1DK58858 and RO1DK54920 (to C. P. K.) and RO1HL57307 and RO1HL63972 (to S. C. R.), the
American Liver Foundation, and the Canadian Institutes of Health
Research (to J. S.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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