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Prostaglandin E 2 modulates dendritic cell function via EP 2 and EP 4 receptor subtypes
Author(s) -
Harizi Hedi,
Grosset Christophe,
Gualde Norbert
Publication year - 2003
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1002483
Subject(s) - prostaglandin e2 receptor , agonist , biology , receptor , medicine , prostaglandin e2 , endocrinology , stimulation , prostaglandin e , adenosine , microbiology and biotechnology , biochemistry
We have reported previously that PGE 2 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 EP 2 R/EP 4 R but not EP 1 R/EP 3 R expressions. NS‐398, a cyclooxygenase (COX)‐2‐selective inhibitor, suppressed LPS‐enhanced EP 2 R/EP 4 R expression, suggesting that COX‐2‐issued prostaglandin E 2 (PGE 2 ) modulates DC function through stimulation of specific EPR subtypes. Using selective agonists, we found that butaprost, an EP 2 R agonist, and PGE 1 alcohol, an EP 2 R and EP 2 R/EP 4 R 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‐ω‐trinor‐PGE 2 , selective agonists for EP 1 R and EP 1 R/EP 3 R, respectively. Treatment of DC with dibutyryl cyclic adenosine monophosphate (cAMP), an analog of cAMP, mimics PGE 2 ‐induced, inhibitory effects. Taken together, our data demonstrate that EP 2 R/EP 4 R are efficient for mediating PGE 2 ‐induced modulation of DC functions.