Expression of prostaglandin E2 receptor 3 in the eyelid epidermis of patients with Stevens-Johnson syndrome/toxic epidermal necrolysis
| Autor: | Tomomichi Nakayama, Akihide Watanabe, Mayumi Ueta, Keiko Yamada, Hiroki Mieno, Shigeru Kinoshita, Chie Sotozono, Yukito Yamanaka |
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| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Pathology medicine.medical_specialty Chemokine medicine.medical_treatment Prostaglandin E2 receptor Inflammation 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine medicine biology business.industry medicine.disease Sensory Systems Toxic epidermal necrolysis Reverse transcription polymerase chain reaction stomatognathic diseases Ophthalmology 030104 developmental biology Cytokine medicine.anatomical_structure 030221 ophthalmology & optometry biology.protein Immunohistochemistry lipids (amino acids peptides and proteins) Eyelid medicine.symptom business |
| Zdroj: | British Journal of Ophthalmology. 104:1022-1027 |
| ISSN: | 1468-2079 0007-1161 |
| Popis: | Background/aimsIn a previous genome-wide association study of Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) patients we reported the association between SJS/TEN and the prostaglandin E receptor 3 (PTGER3) gene, and that its protein PGE2 receptor 3 (EP3) was markedly downregulated in the conjunctival epithelium of SJS/TEN patients. Here we examined EP3 expression of the eyelid epidermis in SJS/TEN patients with severe ocular complications and investigated the function of EP3.MethodsFor the immunohistochemical study, we obtained eyelid samples from five SJS/TEN patients and five patients without SJS/TEN (control subjects) who were undergoing surgery to treat trichiasis, and investigated the expression of EP3 protein in the epidermis of those samples. To investigate the EP3 function in the human epidermal keratinocytes, we performed ELISA and quantitative reverse transcription polymerase chain reaction, since it is reported that PGE2 suppresses cytokine production via EP3 in human conjunctival epithelium.ResultsThe results of the immunohistochemical study revealed that EP3 expression in the eyelid epidermis of the SJS/TEN patients was the same as that in the controls. PGE2 and a selective EP3 agonist suppressed cytokine production and expression induced by polyinosine-polycytidylic acid stimulation, such as chemokine ligand 5 and chemokine motif ligand 10.ConclusionOur findings revealed that in chronic-phase SJS/TEN, EP3 protein was expressed in the eyelid epidermis and was not downregulated, unlike in conjunctival epithelium, and that PGE2 could suppress cytokine production via EP3 in human epidermal keratinocytes. Thus, EP3 expression in the epidermis might contribute to a silencing of skin inflammation in chronic-phase SJS/TEN. |
| Databáze: | OpenAIRE |
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