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Prostaglandin E receptor subtype EP3 downregulates TSLP expression in human conjunctival epithelium
  1. Mayumi Ueta1,2,
  2. Toshiyuki Matsuoka3,
  3. Norihiko Yokoi1,
  4. Shigeru Kinoshita1
  1. 1Department of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan
  2. 2Research Center for Inflammation and Regenerative Medicine, Faculty of Life and Medical Sciences, Doshisha University, Kyoto, Japan
  3. 3Hyogo Prefectural Amagasaki Hospital, Hyogo, Japan
  1. Correspondence to Dr Mayumi Ueta, Department of Ophthalmology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji, Kawaramachi, Kamigyoku, Kyoto 602-0841, Japan; mueta{at}

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Prostanoids are a group of lipid mediators that form in response to various stimuli. They include prostaglandin (PG) D2, PGE2, PGF, PGI2 and thromboxane (TX) A2. There are eight types of prostanoid receptors that are conserved in mammals, ranging from mice to humans: the PGD receptor (DP), four subtypes of the PGE receptor (EP1, EP2, EP3 and EP4), the PGF receptor (FP), the PGI receptor (IP) and the TXA receptor (TP). In regard to PGE receptor subtype EP3, it is reported that the PGE2-EP3 pathway negatively regulates allergic reactions in a murine allergic asthma model1 and that it inhibits keratinocyte activation and exerts anti-inflammatory actions in mouse contact hypersensitivity.2 We also previously reported that PGE2 acts as a ligand for EP3 in murine conjunctival epithelium and downregulates the progression of murine experimental allergic conjunctivitis.3 On the other hand, thymic stromal lymphopoietin (TSLP) plays a key role in allergic inflammation4 and is induced by polyI:C stimulation in epithelial cells, including human conjunctival epithelial cells (HCjECs)5 or keratinocytes. In this study, we examined whether an EP3 agonist could suppress the …

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  • Funding This work was supported in part by grants-in-aid for scientific research from the Japanese Ministry of Health, Labour and Welfare, the Japanese Ministry of Education, Culture, Sports, Science and Technology, CREST from JST, a research grant from the Kyoto Foundation for the Promotion of Medical Science, the Intramural Research Fund of Kyoto Prefectural University of Medicine and a research grant from the Japan Allergy Foundation.

  • Competing interests None.

  • Ethics approval Ethics approval was provided by the institutional review board of Kyoto Prefectural University of Medicine, Kyoto, Japan.

  • Provenance and peer review Not commissioned; externally peer reviewed.