Published online before print May 22, 2003

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(Journal of Leukocyte Biology. 2003;73:756-763.)
© 2003 by Society for Leukocyte Biology

Prostaglandin E₂ modulates dendritic cell function via EP₂ and EP₄ receptor subtypes

Laboratoire d’Immunologie, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 5540, Université de Bordeaux 2, Cedex, France

Correspondence: Dr. Harizi, Laboratoire d’Immunologie, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 5540, Université de Bordeaux 2, 33076 Bordeaux Cedex, France. E-mail: harizi33{at}yahoo.fr

We have reported previously that PGE₂ inhibits dendritic cells (DC) functions. Because E prostanoid receptor (EPR) subtypes involved in this action are unknown, expression and functions of these receptors were examined in DC. Western blot and flow cytometry analyses showed that all EPRs were coexpressed in DC. In a dose-dependent manner, lipopolysaccharide (LPS) enhanced EP₂R/EP₄R but not EP₁R/EP₃R expressions. NS-398, a cyclooxygenase (COX)-2-selective inhibitor, suppressed LPS-enhanced EP₂R/EP₄R expression, suggesting that COX-2-issued prostaglandin E₂ (PGE₂) modulates DC function through stimulation of specific EPR subtypes. Using selective agonists, we found that butaprost, an EP₂R agonist, and PGE₁ alcohol, an EP₂R and EP₂R/EP₄R agonist, inhibited major histocompatibility complex class II expression and enhanced interleukin-10 production from DC. However, no effect was observed with sulprostone and 17-phenyl--trinor-PGE₂, selective agonists for EP₁R and EP₁R/EP₃R, respectively. Treatment of DC with dibutyryl cyclic adenosine monophosphate (cAMP), an analog of cAMP, mimics PGE₂-induced, inhibitory effects. Taken together, our data demonstrate that EP₂R/EP₄R are efficient for mediating PGE₂-induced modulation of DC functions.

Key Words: PGE₂ • EP receptors • agonists • cytokines

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