酒精摄入加剧了实验性自身免疫性前列腺炎,通过肠道微生物群驱动胆固醇生物合成介导的Th17分化
He-Xi Du1, Shao-Yu Yue1, Di Niu1
1Department of Urology, the First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, PR China; Institute of Urology, Anhui Medical University, Hefei, Anhui, PR China; Anhui Province Key Laboratory of Genitourinary Diseases, Anhui Medical University, Hefei, Anhui, PR China.
International immunopharmacology
|July 19, 2024
概括
饮酒会通过改变肠道微生物群和通过胆固醇生物合成增加Th17细胞,使慢性前列腺炎/慢性骨盆疼痛综合征 (CP/CPPS) 恶化. 这项研究揭示了酒精,肠道健康和CP/CPPS进展之间的关键机制.
科学领域:
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
- 胃肠病学 胃肠病学
背景情况:
- 慢性前列腺炎/慢性盆腔疼痛综合征 (CP/CPPS) 是全球普遍存在的疾病.
- 酒精消耗是已知的CP/CPPS风险因素,可能由肠道微生物群和Th17细胞免疫力介导.
研究的目的:
- 阐明酒精加剧CP/CPPS的机制.
- 调查肠道微生物群在酒精诱导的CP/CPPS中的作用.
主要方法:
- 在小鼠中建立了实验性自身免疫性前列腺炎 (EAP) 模型.
- 利用16S rRNA测序和代谢学来分析肠道微生物群和代谢物.
- 在使用27-胆固醇和SREBP2.2进行干预后,评估了Th17细胞分化和前列腺炎的严重程度.
主要成果:
- 酒精摄入增加了Th17细胞比例,炎症因素,肠道透性和改变的肠道微生物群.
- 代谢分析揭示了胆固醇合成途径的失调,在饮酒小鼠中增加了27-胆固醇.
- 用27-基胆固醇补充剂加剧了EAP并促进了Th17分化,由SREBP2调节.
结论:
- 酒精摄入量通过促进Th17细胞分化而加剧EAP.
- 微生物群衍生胆固醇生物合成被确定为酒精诱导的CP/CPPS的关键调解者.
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