Prostaglandin E2 suppresses polyinosine-polycytidylic acid (polyI:C)-stimulated cytokine production via prostaglandin E2 receptor (EP) 2 and 3 in human conjunctival epithelial cells.

BACKGROUND: Prostaglandin (PG) E(2) is produced during inflammatory responses and suppresses the production of cytokines induced by lipopolysaccharide stimulation in macrophages and dendritic cells. In this study, we examined the expression of PGE(2) receptors in human conjunctival epithelial cells and investigated whether PGE(2) downregulates polyinosine-polycytidylic acid (polyI:C)-induced cytokine production.
METHODS: ELISA and quantitative reverse transcription (RT)-PCR were used to examine the effects of PGE(2) on the polyI:C-induced cytokine expressions by primary human conjunctival epithelial cells (PHCjEC). Reverse transcription-PCR was performed to examine the mRNA expression of the PGE(2) receptors EP1, -2, -3 and -4.
RESULTS: PGE(2) significantly attenuated the expressions of chemokine (C-C) motif ligand (CCL) 5, chemokine (C-X-C motif) ligand (CXCL) 10, CXCL11 and interleukin (IL) 6 in PHCjECs. Human conjunctival epithelial cells exhibited expression of EP2, -3 and -4, but not of EP1. EP2 agonist significantly suppressed the polyI:C-induced the expressions of CCL5, CXCL10 and CXCL11 but not of IL-6. EP3 agonist significantly suppressed the expressions of CCL5, CXCL10, CXCL11 and IL-6. On the other hand, EP4 agonist failed to suppress the cytokine production induced by polyI:C stimulation.
CONCLUSION: Our results show that PGE(2) attenuated the expression of CCL5, CXCL10 and CXCL11 via both EP2 and EP3, and that the expression of IL-6 was attenuated only by EP3.