Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1156392 | ENA |
REPOSITORIES: ENA
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Project description:Overactive bladder (OAB) syndrome is a condition that has four symptoms: urgency, urinary frequency, nocturia, and urge incontinence and negatively affects a patient’s life. Recently, it is considered that the urinary bladder urothelium is closely linked to pathogenesis of OAB. However, the mechanisms of pathogenesis of OAB at the molecular level remain poorly understood, mainly as a result of lack of modern molecular analysis. The goal of this study is to identify a potential target protein that could act as a predictive factor for effective diagnosis and aid in the development of therapeutic strategies for the treatment of OAB syndrome. We produced OAB in a rat model and performed the first proteomic analysis on the mucosal layer (urothelium) of the bladders of normal and OAB rats.
2018-02-09 | PXD007571 | Pride
Project description:Fecal Microbiota rawdata from autistic model mice. Female and Male Poly I:C treated mice were compared at microbiota level.
2023-05-04 | E-MTAB-11150 | biostudies-arrayexpress
Project description:<p>Hunner-type interstitial cystitis/bladder pain syndrome (HIC) is a complex and clinically challenging chronic disorder characterized by bladder-centered symptoms, including persistent pelvic pain and urinary urgency frequency, with elusive pathogenesis involving poorly defined multi-system interactions and systemic implications. To investigate upstream drivers of urothelial injury, we employed an integrative multi-omics approach, incorporating metagenomic sequencing, targeted metabolomics of urine and serum, and single-cell RNA sequencing. Our analysis identified Enterococcus avium, Megasphaera micronuciformis, and Fusobacterium nucleatum as the significantly enriched species in HIC patients, with bile acid metabolism appearing as a prominently altered pathway. Metabolomic profiling revealed the elevated levels of taurochenodeoxycholic acid (TCDCA) and tauroursodeoxycholic acid, while single-cell transcriptomic data pointed to TLR3 signaling as a key mediator of urothelial injury. Cross-omics correlation proposed a mechanistic axis involving E. avium, TCDCA, and TLR3 activation. Functional validation using fecal microbiota transplantation, E. avium transplantation, and TCDCA administration demonstrated that this axis contributes to the urothelial barrier disruption and inflammatory responses via TLR3. Intervention with a TLR3 inhibitor demonstrated therapeutic potential. These findings shed light on the pathogenesis of HIC, highlighting the potential role of the gut-bladder axis in disease development. This may contribute not only to the discovery of novel biomarkers but also to the development of personalized treatment strategies targeting specific molecular and microbial pathways.</p>
2025-12-16 | MTBLS13513 | MetaboLights
Project description:The aim of this study is analysis of urinary proteomic pattern in healthy people and patients suffering from OAB symptoms by means of mass spectrophotometry. Establishing characteristic protein profiles, qualitative and quantitative, for OAB will help to define specific protein marker and will allow to develop new investigative protocol enabling to discover at what stage of post-genetic changes urothelium cells change their proteomic profile causing OAB symptoms. Patients will be divided into two groups: group A – OAB patients and group B – control group, without any urinary tract symptoms. All participants will be questionnaired with appropriate tools evaluating quality of life of patients with lower urinary tract symptoms and bladder diary. Urine samples will be taken twice with 7 day gap and then prepared for further evaluation with mass spectrophotometry. Mass spectrophotometry will be performed for all labeled samples with QExactive spectrophotometer. In order to provide maximal credibility and reliability of acquired data each sample will be managed in triplicate. Those result will be analyzed with specific statistical methods and final results will be correlated between the groups. In long-term perspective results of this project will help to understand the underlying pathomechanisms of overactive blabber syndrome. In future those results will be applied for further research in OAB sufferers allowing for precise and objective diagnosis and prognosis. In our opinion it will also serve as a tool for estimations of treatment efficacy of new therapeutic methods. In consequence the project will allow us to create a unique toolkit, combining spectrophotometry, urinary proteomic pattern differences and quality of life correlated with OAB symptoms severity. It will enable to develop new perspectives for overactive bladder pathophysiology research and new therapeutic strategies.
2020-05-12 | PXD017799 | Pride
Project description:<p>Hunner-type interstitial cystitis/bladder pain syndrome (HIC) is a complex and clinically challenging chronic disorder characterized by bladder-centered symptoms, including persistent pelvic pain and urinary urgency frequency, with elusive pathogenesis involving poorly defined multi-system interactions and systemic implications. To investigate upstream drivers of urothelial injury, we employed an integrative multi-omics approach, incorporating metagenomic sequencing, targeted metabolomics of urine and serum, and single-cell RNA sequencing. Our analysis identified <em>Enterococcus avium</em>, <em>Megasphaera micronuciformis</em>, and <em>Fusobacterium nucleatum</em> as the significantly enriched species in HIC patients, with bile acid metabolism appearing as a prominently altered pathway. Metabolomic profiling revealed the elevated levels of taurochenodeoxycholic acid (TCDCA) and tauroursodeoxycholic acid, while single-cell transcriptomic data pointed to TLR3 signaling as a key mediator of urothelial injury. Cross-omics correlation proposed a mechanistic axis involving <em>E. avium</em>, TCDCA, and TLR3 activation. Functional validation using fecal microbiota transplantation, <em>E. avium</em> transplantation, and TCDCA administration demonstrated that this axis contributes to the urothelial barrier disruption and inflammatory responses via TLR3. Intervention with a TLR3 inhibitor demonstrated therapeutic potential. These findings shed light on the pathogenesis of HIC, highlighting the potential role of the gut-bladder axis in disease development. This may contribute not only to the discovery of novel biomarkers but also to the development of personalized treatment strategies targeting specific molecular and microbial pathways.</p>
2025-12-16 | MTBLS13512 | MetaboLights
Project description:Healthy human and mouse colon epithelium is a major source of active thrombin, released in lumen. Using germ-free animals, we demonstrated that mucosal thrombin was directly regulated by the presence of commensal microbiota. Specific inhibition of lumenal thrombin activity caused macro-, microscopic damage and transcriptomic alterations of genes involved in host-microbiota interactions. Further, lumenal thrombin inhibition impaired the spatial segregation of microbiota biofilms, allowing bacteria to invade the mucus layer and to translocate across the epithelium. Thrombin proteolyzed the biofilm matrix of reconstituted mucosa-associated human microbiota. We demonstrated a previously unknown physiological role for epithelial thrombin that constrains biofilms at mucosal surfaces. We report that lung, bladder and skin epithelia also expressed thrombin, suggesting that this role may be applicable to other host-microbiome surfaces. Our discovery points route to new therapies targeting biofilms, important for a broad range of disorders, in the gut, and beyond.
2019-06-24 | PXD014315 | Pride
Project description:Hunner-type interstitial cystitis/bladder pain syndrome (HIC) is a complex and clinically challenging chronic disorder characterized by bladder-centered symptoms, including persistent pelvic pain and urinary urgency frequency, with elusive pathogenesis involving poorly defined multi-system interactions and systemic implications. To investigate upstream drivers of urothelial injury, we employed an integrative multi-omics approach, incorporating metagenomic sequencing, targeted metabolomics of urine and serum, and single-cell RNA sequencing. Our analysis identified Enterococcus avium, Megasphaera micronuciformis, and Fusobacterium nucleatum as the significantly enriched species in HIC patients, with bile acid metabolism appearing as a prominently altered pathway. Metabolomic profiling revealed the elevated levels of taurochenodeoxycholic acid (TCDCA) and tauroursodeoxycholic acid, while single-cell transcriptomic data pointed to TLR3 signaling as a key mediator of urothelial injury. Cross-omics correlation proposed a mechanistic axis involving E. avium, TCDCA, and TLR3 activation. Functional validation using fecal microbiota transplantation, E. avium transplantation, and TCDCA administration demonstrated that this axis contributes to the urothelial barrier disruption and inflammatory responses via TLR3. Intervention with a TLR3 inhibitor demonstrated therapeutic potential. These findings shed light on the pathogenesis of HIC, highlighting the potential role of the gut-bladder axis in disease development. This may contribute not only to the discovery of novel biomarkers but also to the development of personalized treatment strategies targeting specific molecular and microbial pathways.
2025-11-21 | GSE310557 | GEO
Project description:Use of Fermented Red Clover Isoflavones in the Treatment of Overactive Bladder, focusing on vaginal and urine microbiota
| PRJNA1075925 | ENA