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Regulatory effect of 17β-estradiol on the expression of β-defensin-2 and proinflammatory cytokines in human oral epithelial cells

Wu T1,2,3Tang C1,2,3Chen Y1,3Yong X1,3Liu Z1Jiang L1,2Zeng Q1,3Tao R1,2,3.

J Oral Pathol Med. 2020 Mar 16. doi: 10.1111/jop.13016. [Epub ahead of print]




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.


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 M ICI182,780 or 10-7 M G1 for 1 h, E2 (10-7 M, 10-8 M, 10-9 M) for 36 h, 100ng/ml IL-1β for 12 h, 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.


Expression of hBD-2 and inflammatory cytokines increased after IL-1β stimulation, which was down-regulated by E2 pretreatment. With ICI182,780, the suppression of E2 on hBD-2 mRNA was attenuated. With G1, the mRNA and protein expression of hBD-2 were reduced.


Pretreatment 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.