尿道致病性菌群失调模式与尿道纤维化有关

Michael Witthaus, Saager Chawla, Dhruvi Puri, Kyoko Sakamoto, Jill Buckley, Aaron Miller, Mahadevan Rajasekaran
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引用次数: 1

摘要

反复经尿道干预后狭窄进展的细胞机制尚不清楚。我们假设尿道损伤和机械拉伸导致尿道上皮细胞撕裂,导致上皮渗漏和尿液外渗。尿中细菌穿过上皮,可能通过微生物活动引起的炎症促进纤维生成。我们的目的是使用16S rRNA和霰弹枪宏基因组测序分析对尿道狭窄疾病患者和健康对照者的尿组进行病例对照研究,以阐明尿组在尿道狭窄进展中的临床相关性。首先收集患者和健康志愿者的尿液样本,用尿液颗粒提取DNA,然后进行高通量16S rRNA和霰弹枪宏基因组测序。测序数据用于确定与尿道狭窄疾病相关的微生物分类群和功能。测序结果显示,尿道狭窄疾病患者与健康对照组的下尿路尿组存在显著差异。特别是,分类学和代谢谱表明,克雷伯氏菌是一种已知的尿路病原体,耐抗生素物种形成厌氧生物膜。重要的是,研究中没有患者表现出临床感染的体征或症状。我们的研究结果表明,尿路病原体如克雷伯氏菌在炎症环境和随后的纤维化进展中形成生物膜的作用。未来的研究将阐明克雷伯菌诱导纤维化的具体机制。我们的数据表明,针对特定细菌或生物膜的形成可能有利于尿道狭窄疾病的检测和预防进展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Uropathogenic Dysbiosis Pattern is Associated With Urethral Fibrosis
Cellular mechanisms of stricture progression after repeated transurethral interventions are unclear. We hypothesize that urethral injury and mechanical stretch cause tears on the urethral epithelial cell lining leading to leaking epithelium and urine extravasation. Urinary bacteria traverse the epithelial lining and may promote fibrogenesis through inflammation due to microbial activity. Our objective was to perform a case-control study of the urobiome from patients with urethral stricture disease or healthy controls using 16S rRNA and shotgun metagenomic sequencing profiling to elucidate the clinical relevance of the urobiome in urinary stricture progression. First catch urine samples from patients and healthy volunteers were collected and pelleted urine was used for DNA extraction, followed by high throughput 16S rRNA and shotgun metagenomic sequencing. Sequencing data were used to determine microbial taxa and functions associated with urethral stricture disease. Sequencing results revealed that the lower urinary tract urobiome was significantly different between urethral stricture disease cases and healthy controls. In particular, taxonomic and metabolic profiles point toward anaerobic biofilm formation by antibiotic-resistant species of Klebsiella, which is a known uropathogen. Importantly, no patients in the study exhibited signs or symptoms of clinical infection. Our findings suggest a role for biofilm formation by uropathogens such as Klebsiella spp. in developing an inflammatory environment and consequent fibrosis progression. Future studies will elucidate specific mechanisms of Klebsiella-induced fibrosis. Our data suggest that targeting specific bacteria or biofilm formation may be beneficial for urethral stricture disease detection and prevention of progression.
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