Prenatal dexamethasone and postnatal high-fat diet decrease interferon gamma production through an age-dependent histone modification in male sprague-dawley rats

Hong Ren Yu, You Lin Tain, Jiunn Ming Sheen, Mao Meng Tiao, Chih Cheng Chen, Ho Chang Kuo, Pi Lien Hung, Kai Sheng Hsieh, Li Tung Huang*

*此作品的通信作者

研究成果: 期刊稿件文章同行評審

17 引文 斯高帕斯(Scopus)

摘要

Overexposure to prenatal glucocorticoid (GC) disturbs hypothalamic-pituitary-adrenocortical axis-associated neuroendocrine metabolism and susceptibility to metabolic syndrome. A high-fat (HF) diet is a major environmental factor that can cause metabolic syndrome. We aimed to investigate whether prenatal GC plus a postnatal HF diet could alter immune programming in rat offspring. Pregnant Sprague-Dawley rats were given intraperitoneal injections of dexamethasone or saline at 14-21 days of gestation. Male offspring were then divided into four groups: vehicle, prenatal dexamethasone exposure, postnatal HF diet (VHF), and prenatal dexamethasone exposure plus a postnatal HF diet (DHF). The rats were sacrificed and adaptive immune function was evaluated. Compared to the vehicle, the DHF group had lower interferon gamma (IFN-γ) production by splenocytes at postnatal day 120. Decreases in H3K9 acetylation and H3K36me3 levels at the IFN-γ promoter correlated with decreased IFN-γ production. The impaired IFN-γ production and aberrant site-specific histone modification at the IFN-γ promoter by prenatal dexamethasone treatment plus a postnatal HF diet resulted in resilience at postnatal day 180. Prenatal dexamethasone and a postnatal HF diet decreased IFN-γ production through a site-specific and an age-dependent histone modification. These findings suggest a mechanism by which prenatal exposure to GC and a postnatal environment exert effects on fetal immunity programming.

原文英語
文章編號1610
期刊International Journal of Molecular Sciences
17
發行號10
DOIs
出版狀態已出版 - 10 2016

文獻附註

Publisher Copyright:
© 2016 by the authors; licensee MDPI, Basel, Switzerland.

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