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Regulatory effect of 17β‐estradiol on the expression of β‐defensin‐2 and proinflammatory cytokines in human oral epithelial cells
Author(s) -
Wu Tiantian,
Tang Caijin,
Chen Yi,
Yong Xiangzhi,
Liu Zhenmin,
Jiang Lanlan,
Zeng Qixin,
Tao Renchuan
Publication year - 2020
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.13016
Subject(s) - proinflammatory cytokine , endocrinology , medicine , tumor necrosis factor alpha , interleukin , estrogen , estrogen receptor , western blot , receptor , messenger rna , inflammation , gper , cytokine , beta defensin , biology , innate immune system , biochemistry , gene , cancer , breast cancer
Background Although estrogen deficiency has been proposed as a risk factor for oral mucosal inflammatory diseases in post‐menopausal women, the mechanisms involved remain unclear. This study aimed to investigate the effect of 17β‐estradiol (E2) on the inflammatory response stimulated by interleukin‐1 beta (IL‐1β) in human oral mucosal epithelial cells (hOMECs) and its possible mechanism. Methods Primary hOMECs were obtained from female infants and cultured in keratinocyte growth medium. The hOMECs at second passage were collected and stimulated by 10 −7 mol/L ICI182,780 or 10 −7 mol/L G1 for 1 hour, E2 (10 −7 mol/L, 10 −8 mol/L, 10 −9 mol/L) for 36 hour, 100 ng/mL IL‐1β for 12 hours, respectively. Human beta‐2 defensin (hBD‐2), tumor necrosis factor‐alpha (TNF)‐α, IL‐6, IL‐8, estrogen receptor‐alpha (ERα), estrogen receptor‐beta (ERβ), and G protein‐coupled receptor 30 (GPR30) mRNA levels and protein levels were measured by real‐time quantitative polymerase chain reaction (RT‐qPCR), enzyme‐linked immunosorbent assay (ELISA), and Western Blot (WB), respectively. Results Expression of hBD‐2 and inflammatory cytokines increased after IL‐1β stimulation, which was down‐regulated by E2 pre‐treatment. With ICI182,780, the suppression of E2 on hBD‐2 mRNA was attenuated. With G1, the mRNA expression and protein expression of hBD‐2 were reduced. Conclusion Pre‐treatment of hOMECs with E2 at physiological concentrations inhibited the IL‐1β‐induced expression of hBD‐2 and inflammatory cytokines. The protective effects of E2 suggest its potential use treating oral inflammatory diseases in clinical practice.