Downregulation of Monocyte Chemoattractant Protein 1 Expression by Prostaglandin E2 in Human Ocular Surface Epithelium | Genetics and Genomics | JAMA Ophthalmology | JAMA Network
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Research Letter
Feb 2012

Downregulation of Monocyte Chemoattractant Protein 1 Expression by Prostaglandin E2 in Human Ocular Surface Epithelium

Author Affiliations

Author Affiliations: Research Center for Inflammation and Regenerative Medicine, Faculty of Life and Medical Sciences, Doshisha University (Dr Ueta) and Department of Ophthalmology, Kyoto Prefectural University of Medicine (Drs Ueta, Sotozono, Yokoi, and Kinoshita), Kyoto, Japan.

Arch Ophthalmol. 2012;130(2):249-251. doi:10.1001/archopthalmol.2011.1472

Elsewhere, we reported that in the tears and serum of patients with acute-stage Stevens-Johnson syndrome or toxic epidermal necrolysis, the levels of interleukin 6 (IL-6), IL-8, and monocyte chemoattractant protein 1 (MCP-1) were dramatically increased.1 We also reported that Stevens-Johnson syndrome or toxic epidermal necrolysis with severe ocular complications was associated with polymorphism of the prostaglandin E receptor 3 (EP3) gene (PTGER3).2

Prostanoids are a group of lipid mediators that form in response to various stimuli. They include prostaglandin D2 (PGD2), PGE2, PGF, PGI2, and thromboxane A2. There are 4 subtypes of the PGE receptor: EP1, EP2, EP3, and EP4. We previously reported that PGE2 suppresses polyinosine–polycytidylic acid (polyI:C)–stimulated cytokine production via EP2 and/or EP3 in human ocular surface epithelial cells.3,4 PolyI:C is a ligand of Toll-like receptor 3, which is strongly expressed in ocular surface epithelium.5 We found that PGE2 suppresses the production of IL-6, chemokine (C-X-C motif) ligand 10, chemokine (C-X-C motif) ligand 11, and chemokine (C-C motif) ligand 5 but not IL-8 by epithelial cells on the human ocular surface3; it remains to be determined whether it also suppresses MCP-1 production. Monocyte chemoattractant protein 1 plays a significant role in the recruitment of monocytes and lymphocytes to the site of cellular immune reactions. In this study, we investigated whether PGE 2 downregulates polyI:C-induced MCP-1 production.

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