Prostaglandin E2 suppresses polyinosine-polycytidylic acid (polyI:C)-stimulated cytokine production via prostaglandin E2 receptor (EP) 2 and 3 in human conjunctival epithelial cells
Prostaglandin E2 suppresses polyinosine-polycytidylic acid (polyI:C)-stimulated cytokine production via prostaglandin E2 receptor (EP) 2 and 3 in human conjunctival epithelial cells
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DOI：
10.1136/bjo.2010.199679
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发表时间：
2011-06-01
影响因子：
4.1
通讯作者：
Kinoshita, Shigeru
中科院分区：
文献类型：
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作者：
Ueta, Mayumi;Matsuoka, Toshiyuki;Kinoshita, Shigeru
前列腺素E-2在炎症反应中产生，并抑制巨噬细胞和树突状细胞中脂多糖刺激诱导的细胞因子的产生。方法采用ELISA和定量逆转录PCR方法检测PGE（2）对polyI：C诱导的原代人结膜上皮细胞（PHCjEC）细胞因子表达的影响。结果PGE（2）可明显抑制PHCjECs趋化因子（C-C）基序配体（CCL）5、趋化因子（C-X-C基序）配体（CXCL）10、CXCL 11和白细胞介素（IL）6的表达。人结膜上皮细胞表现出EP 2、-3和-4的表达，但不表达EP 1。EP 2激动剂显著抑制polyI：C诱导的CCL 5、CXCL 10和CXCL 11的表达，但不抑制IL-6的表达。EP 3激动剂可显著抑制CCL 5、CXCL 10、CXCL 11和IL-6的表达。结论PGE（2）通过EP 2和EP 3抑制CCL 5、CXCL 10和CXCL 11的表达，而EP 3仅抑制IL-6的表达。
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.