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Inflammation characteristics in bladder pain syndrome ESSIC type 3C/classic interstitial cystitis
Department of Urology, Sahlgrenska University Hospital, Gothenburg, Sweden.
Örebro University, School of Medicine, Örebro University, Sweden.
Department of Rheumatology and Inflammation Research, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Sahlgrenska University Hospital, Gothenburg, Sweden.
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2014 (English)In: International journal of urology, ISSN 0919-8172, E-ISSN 1442-2042, Vol. 21, no Suppl. 1, p. 75-78Article in journal (Refereed) Published
Abstract [en]

Objectives: Interstitial cystitis is regarded as a heterogenous syndrome with two distinguishable forms: the non-ulcer and the classic form of interstitial cystitis, the latter with Hunner's lesions; or bladder pain syndrome type 3C and non-Hunner bladder pain syndrome, respectively.

Methods: A cohort of 379 patients diagnosed with interstitial cystitis was studied. Nitric oxide release from the bladder was measured using a chemiluminescence nitric oxide analyzer. Bladder biopsies from the patients and healthy controls were analyzed by routine histopathological examination. Biopsies from a subset of patients and controls were also analyzed by immunohistochemistry and cytokine gene expression by real-time polymerase chain reaction.

Results: Patients with bladder pain syndrome type 3C/classic interstitial cystitis had considerably higher levels of nitric oxide as compared with non-Hunner bladder pain syndrome/non-ulcer interstitial cystitis patients and healthy individuals, and showed histologically a chronic inflammation in the bladder mucosa, with abundant mast cell infiltration in all layers of the bladder wall. No inflammation was noted in non-Hunner bladder pain syndrome/non-ulcer interstitial cystitis patients. The isoenzymes inducible nitric oxide synthase, the catalyst in the nitric oxide production, was strongly expressed in the inflammatory cells in the bladder mucosa of bladder pain syndrome type 3C/classic interstitial cystitis patients. In addition, the expression of the pro-inflammatory cytokines interleukin-6 and interleukin-17A messenger ribonucleic acid, and of anti-inflammatory interleukin-10 messenger ribonucleic acid showed significantly increased levels in bladder pain syndrome type 3C/classic interstitial cystitis compared with healthy controls.

Conclusion: Bladder pain syndrome type 3C/classic interstitial cystitis is a distinct inflammatory disease and in many aspects shares features of inflammatory autoimmune diseases. These findings could open up novel research avenues with expectations for new targets for pharmacological treatment.

Place, publisher, year, edition, pages
Hoboken: Wiley-Blackwell, 2014. Vol. 21, no Suppl. 1, p. 75-78
Keywords [en]
Bladder pain syndrome, cytokine, inducible nitric oxide synthase, inflammatory mediators, interstitial cystitis, nitric oxide
National Category
Urology and Nephrology
Research subject
Medicine
Identifiers
URN: urn:nbn:se:oru:diva-35825DOI: 10.1111/iju.12370ISI: 000335491500079PubMedID: 24807505Scopus ID: 2-s2.0-84899803856OAI: oai:DiVA.org:oru-35825DiVA, id: diva2:740672
Note

Funding Agencies:

University of Gothenburg ALF

Anna-Lisa and Bror Björnssons Research Foundation

Martha and Gustaf Ågrens Research Foundation

Örebro University

Available from: 2014-08-26 Created: 2014-07-30 Last updated: 2017-12-05Bibliographically approved

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Delbro, Dick

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