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

IF 1.6 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
American journal of translational research Pub Date : 2025-08-15 eCollection Date: 2025-01-01 DOI:10.62347/CRGN1110
Xin Zhu, Ping Xu, Yandong He, Wenlong Lu, Zhong Wang, Feng Liu
{"title":"Alcohol promoted prostate microbial imbalance in the rat model of prostatitis.","authors":"Xin Zhu, Ping Xu, Yandong He, Wenlong Lu, Zhong Wang, Feng Liu","doi":"10.62347/CRGN1110","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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 <i>Streptomyces, Oscillospira, Pseudomonas, Lactobacillus</i>, unidentified-<i>Clostridiales</i>, and unclassified-Bacteria.</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":7731,"journal":{"name":"American journal of translational research","volume":"17 8","pages":"5914-5927"},"PeriodicalIF":1.6000,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12432687/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"American journal of translational research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.62347/CRGN1110","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0

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 Streptomyces, Oscillospira, Pseudomonas, Lactobacillus, unidentified-Clostridiales, 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.

酒精促进前列腺炎模型大鼠前列腺微生物失衡。
目的:酒精可加重慢性前列腺炎(CP)/慢性盆腔疼痛综合征(CPPS)的临床症状,但其分子机制尚不完全清楚。在我们的研究中,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:用前列腺类固醇结合蛋白建立EAP大鼠模型,随后给予酒精暴露。酒精浓度用标准酒精浓度测定法测定。采用酶联免疫吸附法(ELISA)检测炎症因子。随后,利用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:炎性因子水平升高及前列腺组织形态学特征证实EAP大鼠模型建立成功。酒精暴露后,血液中酒精浓度显著升高。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、均匀性和组成。预计与生物合成、降解/利用/同化、解毒、前列腺代谢物和能量的产生、大分子修饰、聚糖途径和代谢簇相关的50多种代谢途径将被破坏。此外,代谢组学分析显示,酒精损伤了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,包括链霉菌、示波螺旋体、假单胞菌、乳杆菌、未鉴定的梭状芽孢杆菌和未分类的细菌。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而加剧前列腺炎。这一发现可为改善酒精性前列腺炎的诊断和治疗提供有价值的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
American journal of translational research
American journal of translational research ONCOLOGY-MEDICINE, RESEARCH & EXPERIMENTAL
自引率
0.00%
发文量
552
期刊介绍: Information not localized
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信