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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]

 

Abstract

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 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.

RESULTS:

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.

CONCLUSION:

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.