Purchase this article with an account.
Mayumi Ueta, Toshiyuki Matsuoka, Norihiko Yokoi, Shigeru Kinoshita; Prostaglandin E2 Suppresses Polyi:c-stimulated Cytokine Production Via EP2 And EP3 In Human Conjunctival Epithelial Cells. Invest. Ophthalmol. Vis. Sci. 2011;52(14):2583.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
PGE2 is produced during inflammatory responses and suppresses the production of cytokines and chemokines induced by LPS stimulation in macrophages and dendritic cells. Human corneal and conjunctival epithelial cells produce cytokines such as IL-6, IL-8, and IFN-β in response to stimulation by polyI:C but not LPS. In this study, we examined the expression of PGE2 receptors in human conjunctival epithelial cells and investigated whether PGE2 down-regulates polyI:C-induced cytokine production.
We used ELISA and quantitative RT-PCR assay to examine the effects of PGE2 on the polyI:C-induced production and mRNA expression of IL-6, IL-8, CCL5, CXCL10, and CXCL11 by primary human conjunctival epithelial cells (PHCjEC). We performed RT-PCR to assay the mRNA expression of the PGE2 receptor EP1-4 in human conjunctival epithelial cells.
PGE2 significantly attenuated the productions and mRNA expressions of CCL5, CXCL10, CXCL11, and IL-6 but not of IL-8. PHCjECs and in vivo human conjunctival epithelial cells expressed the mRNA expression of EP2, EP3, and EP4, but not for EP1. EP2 agonist significantly suppressed the polyI:C-induced production and mRNA expressions of CCL5, CXCL10, and CXCL11 but not of IL-6. EP3 agonist significantly suppressed the production and mRNA 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.
Our results show that PGE2 attenuated the mRNA expression and production of CCL5, CXCL10, and CXCL11 via both EP2 and EP3, and that the IL-6 mRNA expression and production of IL-6 was attenuated only by EP3.
This PDF is available to Subscribers Only