{"title":"The role of the urinary microbiome in diabetes-associated UTIs: current understanding and future directions.","authors":"Meenakshi Reddy Yathindra, Rithvika Badugu, Shaurya Kumar Singh, Sowthrisha Paluri, Hrudai Poudala, Naraginti Leninbabu Swathi","doi":"10.1515/jbcpp-2025-0116","DOIUrl":null,"url":null,"abstract":"<p><p>This review explores the interplay between type 2 diabetes mellitus (T2DM) and urinary microbiome dysbiosis, focusing on its role in urinary tract infections (UTIs). Once considered sterile, the urinary tract hosts a diverse microbiota that supports mucosal immunity and pathogen resistance. In T2DM, chronic hyperglycemia and glycosuria disrupt microbial balance, impair immune responses, and increase UTI susceptibility. Glycosuria promotes pathogenic colonization, biofilm formation, and microbial shifts, with studies reporting a threefold rise in <i>Escherichia coli</i> and a 56 % reduction in <i>Lactobacillus</i> spp. in diabetic women with recurrent UTIs. Diabetic urine shows reduced diversity, higher abundance of <i>Klebsiella</i>, <i>Pseudomonas</i>, and <i>Enterococcus</i>, and elevated IL-8. Microbiota-targeted interventions, including probiotics (<i>Lactobacillus crispatus</i>, <i>Lactobacillus rhamnosus</i> GR-1), prebiotics (astaxanthin), and phytotherapeutics (cranberry), demonstrate potential via lactic acid, hydrogen peroxide production, competitive exclusion, and NF-κB modulation. A 12-month RCT showed significant UTI recurrence reduction with probiotics. Advances in 16 S rRNA sequencing and metagenomics reveal microbial signatures associated with diabetic UTIs, though methodological heterogeneity limits comparability. A review of 1,200 publications (2000-2024) highlights the need for longitudinal studies and precision microbiota therapeutics to translate findings into clinical practice.</p>","PeriodicalId":15352,"journal":{"name":"Journal of Basic and Clinical Physiology and Pharmacology","volume":" ","pages":"9-24"},"PeriodicalIF":0.0000,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Basic and Clinical Physiology and Pharmacology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1515/jbcpp-2025-0116","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"Pharmacology, Toxicology and Pharmaceutics","Score":null,"Total":0}
引用次数: 0
Abstract
This review explores the interplay between type 2 diabetes mellitus (T2DM) and urinary microbiome dysbiosis, focusing on its role in urinary tract infections (UTIs). Once considered sterile, the urinary tract hosts a diverse microbiota that supports mucosal immunity and pathogen resistance. In T2DM, chronic hyperglycemia and glycosuria disrupt microbial balance, impair immune responses, and increase UTI susceptibility. Glycosuria promotes pathogenic colonization, biofilm formation, and microbial shifts, with studies reporting a threefold rise in Escherichia coli and a 56 % reduction in Lactobacillus spp. in diabetic women with recurrent UTIs. Diabetic urine shows reduced diversity, higher abundance of Klebsiella, Pseudomonas, and Enterococcus, and elevated IL-8. Microbiota-targeted interventions, including probiotics (Lactobacillus crispatus, Lactobacillus rhamnosus GR-1), prebiotics (astaxanthin), and phytotherapeutics (cranberry), demonstrate potential via lactic acid, hydrogen peroxide production, competitive exclusion, and NF-κB modulation. A 12-month RCT showed significant UTI recurrence reduction with probiotics. Advances in 16 S rRNA sequencing and metagenomics reveal microbial signatures associated with diabetic UTIs, though methodological heterogeneity limits comparability. A review of 1,200 publications (2000-2024) highlights the need for longitudinal studies and precision microbiota therapeutics to translate findings into clinical practice.
本文综述了2型糖尿病(T2DM)与尿微生物群失调之间的相互作用,重点讨论了其在尿路感染(uti)中的作用。一旦被认为是无菌的,泌尿道拥有多种微生物群,支持粘膜免疫和病原体抵抗。在T2DM中,慢性高血糖和糖尿会破坏微生物平衡,损害免疫反应,增加尿路感染的易感性。糖尿促进致病性定植、生物膜形成和微生物转移,研究报告在复发性尿路感染的糖尿病妇女中,大肠杆菌增加三倍,乳酸杆菌减少56% %。糖尿病患者尿液多样性降低,克雷伯氏菌、假单胞菌和肠球菌丰度增高,白细胞介素-8升高。以微生物群为目标的干预措施,包括益生菌(crispatus乳杆菌、鼠李糖乳杆菌GR-1)、益生元(虾青素)和植物疗法(蔓越莓),通过乳酸、过氧化氢生产、竞争排斥和NF-κB调节显示出潜力。一项为期12个月的随机对照试验显示,益生菌显著减少了尿路感染的复发。16 S rRNA测序和宏基因组学的进展揭示了与糖尿病尿路感染相关的微生物特征,尽管方法异质性限制了可比性。对1200份出版物(2000-2024)的回顾强调了纵向研究和精确微生物群治疗的必要性,以将研究结果转化为临床实践。
期刊介绍:
The Journal of Basic and Clinical Physiology and Pharmacology (JBCPP) is a peer-reviewed bi-monthly published journal in experimental medicine. JBCPP publishes novel research in the physiological and pharmacological sciences, including brain research; cardiovascular-pulmonary interactions; exercise; thermal control; haematology; immune response; inflammation; metabolism; oxidative stress; and phytotherapy. As the borders between physiology, pharmacology and biochemistry become increasingly blurred, we also welcome papers using cutting-edge techniques in cellular and/or molecular biology to link descriptive or behavioral studies with cellular and molecular mechanisms underlying the integrative processes. Topics: Behavior and Neuroprotection, Reproduction, Genotoxicity and Cytotoxicity, Vascular Conditions, Cardiovascular Function, Cardiovascular-Pulmonary Interactions, Oxidative Stress, Metabolism, Immune Response, Hematological Profile, Inflammation, Infection, Phytotherapy.