ArticleInflammation2017
An Immunogenic Peptide, T2 Induces Interstitial Cystitis/Painful Bladder Syndrome: an Autoimmune Mouse Model for Interstitial Cystitis/Painful Bladder Syndrome.
Article in Inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- An indirect comparison meta-analysis of noninvasive intravesical instillation and intravesical injection of botulinum toxin-A in bladder disorders.International urology and nephrology · 2022Pooled it
- Animal Models of Hunner-Type Interstitial Cystitis.International journal of urology : official journal of the Japanese Urological Association · 2026Review
- Experimental murine models of interstitial cystitis/bladder pain syndrome: A review.Histology and histopathology · 2025Review
- Role of local angiotensin II signaling in bladder function.American journal of physiology. Renal physiology · 2024Review
- Review
- The Roles of T cells in Bladder Pathologies.Trends in immunology · 2021Review
- Autoimmunity to urothelial antigen causes bladder inflammation, pelvic pain, and voiding dysfunction: a novel animal model for Hunner-type interstitial cystitis.American journal of physiology. Renal physiology · 2021Article
- Interstitial cystitis/bladder pain syndrome: The evolving landscape, animal models and future perspectives.International journal of urology : official journal of the Japanese Urological Association · 2020Review
- Article
- An update on treatment options for interstitial cystitis.Przeglad menopauzalny = Menopause review · 2020Review
- Construction and application of urinary system model with functional bladder module.Saudi journal of biological sciences · 2019Article
- Increased Piezo1 channel activity in interstitial Cajal-like cells induces bladder hyperactivity by functionally interacting with NCX1 in rats with cyclophosphamide-induced cystitis.Experimental & molecular medicine · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The exact pathophysiology of interstitial cystitis/painful bladder syndrome is unknown; however, autoimmunity is a valid theory. We developed an autoimmune chronic cystitis model by administration of the medium dose of immunogenic peptide T2. Sixty female C57BL/6 mice were divided into six groups. The control group was not treated with any reagent. CFA group was injected with CFA + normal saline, homogenate group with bladder homogenate + CFA, low-dose group with low dose of T2 peptide + CFA, medium dose group with the medium dose of T2 peptide + CFA, and high-dose group with the high dose of T2 peptide + CFA. Micturition habits, withdrawal frequencies of mice, and bladders weight were measured for each group. Hematoxylin and eosin staining and toluidine blue staining were used to investigate bladder inflammation and mast cells accumulation, respectively. T cells infiltration in the bladder tissues and serum TNF-α level were measured by using immunohistochemistry and ELISA, respectively. Mice immunized with the medium dose of T2 peptide (0.225 mg/ml) were extremely sensitive to the applied force, showed greater urine frequencies, and higher bladder weights. Histologic examination revealed severe edema and inflammation in bladder tissues of medium-dose group. Extensive infiltration of T cells in bladder tissues, elevated TNF-α, and increased mast cells accumulation were observed in medium-dose group as compared to that in other groups. EAC mice model established by injecting the medium dose of T2 (0.225 mg/ml) mimics all the symptoms and pathophysiologic characteristics of IC/PBS. We believe that this model can help us to investigate the pathogenesis of IC/PBS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.