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酒精在前列腺炎大鼠模型中促进了前列腺微生物失衡。

Alcohol promoted prostate microbial imbalance in the rat model of prostatitis.

作者信息

Zhu Xin, Xu Ping, He Yandong, Lu Wenlong, Wang Zhong, Liu Feng

机构信息

Department of Urology, Shanghai Fengxian District Central Hospital, Urology Specialty Alliance of Fengxian District Shanghai, P. R. China.

Department of Nursing, Shanghai Fengxian District Central Hospital Shanghai, P. R. China.

出版信息

Am J Transl Res. 2025 Aug 15;17(8):5914-5927. doi: 10.62347/CRGN1110. eCollection 2025.

Abstract

OBJECTIVE

Alcohol may aggravate the clinical symptoms of chronic prostatitis (CP)/chronic pelvic pain syndrome (CPPS), but the molecular mechanism behind this connection have not been fully understood. In our study, we established a rat model of experimental autoimmune prostatitis (EAP) to investigate the impact of alcohol exposure on the changes in prostatic microbiota.

METHODS

The EAP rat model was established using prostate steroid-binding protein with subsequently administered alcohol exposure. The concentration of alcohol was quantified by a standard alcohol concentration assay. The inflammatory factors were measured through enzyme-linked immunosorbent assay (ELISA). Subsequently, the composition and diversity of the prostate microbiota were analyzed using 16S rRNA gene sequencing data.

RESULTS

Elevated levels of inflammatory factors and morphological characteristics of prostate tissue confirmed that the EAP rat model was successfully established. Following alcohol exposure, a significant increase in blood alcohol concentration was observed. Alcohol exposure further exacerbated dysbiosis in prostate microbiota, altering microbial abundance, evenness, and composition in EAP rats. More than 50 metabolic pathways related to biosynthesis, degradation/utilization/assimilation, detoxification, generation of prostate metabolite and energy, macromolecule modification, glycan pathways and metabolic clusters were predicted to be disrupted. Additionally, metabolomics profiling revealed that alcohol impaired pathways such as PWY-6876, PWY-6339, PWY-722, and PWY-5177, which were strongly associated with microbial changes, including , unidentified-, and unclassified-Bacteria.

CONCLUSION

Our findings suggested that alcohol exacerbates prostatitis by disrupting the balance of prostate microbiota. This finding could provide valuable insights for improving the diagnosis and treatment for patients with alcoholic prostatitis.

摘要

目的

酒精可能会加重慢性前列腺炎(CP)/慢性盆腔疼痛综合征(CPPS)的临床症状,但其背后的分子机制尚未完全明确。在本研究中,我们建立了实验性自身免疫性前列腺炎(EAP)大鼠模型,以研究酒精暴露对前列腺微生物群变化的影响。

方法

采用前列腺类固醇结合蛋白建立EAP大鼠模型,随后进行酒精暴露。通过标准酒精浓度测定法定量酒精浓度。通过酶联免疫吸附测定(ELISA)测量炎症因子。随后,使用16S rRNA基因测序数据分析前列腺微生物群的组成和多样性。

结果

炎症因子水平升高及前列腺组织的形态学特征证实EAP大鼠模型成功建立。酒精暴露后,血液酒精浓度显著升高。酒精暴露进一步加剧了前列腺微生物群的失调,改变了EAP大鼠的微生物丰度、均匀度和组成。预计超过50条与生物合成、降解/利用/同化、解毒、前列腺代谢物和能量生成、大分子修饰、聚糖途径和代谢簇相关的代谢途径会受到破坏。此外,代谢组学分析显示,酒精损害了PWY - 6876、PWY - 6339、PWY - 722和PWY - 5177等途径,这些途径与微生物变化密切相关,包括未鉴定的、未分类的细菌。

结论

我们的研究结果表明,酒精通过破坏前列腺微生物群的平衡加重前列腺炎。这一发现可为改善酒精性前列腺炎患者的诊断和治疗提供有价值的见解。

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