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, PGF2α, 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.