title: Inflammation characteristics in bladder pain syndrome ESSIC type 3C/classic interstitial cystitis.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Urology, Sahlgrenska University Hospital, Gothenburg, Sweden.
authors.forename: Yr
authors.initials: Y
authors.lastname: Logadottir
authors.forename: Dick
authors.initials: D
authors.lastname: Delbro
authors.forename: Catharina
authors.initials: C
authors.lastname: Lindholm
authors.forename: Magnus
authors.initials: M
authors.lastname: Fall
authors.forename: Ralph
authors.initials: R
authors.lastname: Peeker
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D001706:Biopsy; D018856:Cystitis, Interstitial / Q000145:classification / Q000175:diagnosis / Q000378:metabolism; D003558:Cystoscopy / Q000379:methods; D003627:Data Interpretation, Statistical; D005260:Female; D015870:Gene Expression; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000378:metabolism / Q000473:pathology; D007378:Interleukins / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism / Q000652:urine; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism*; D001743:Urinary Bladder / Q000378:metabolism / Q000473:pathology
chemical_list: D015415:Biomarkers; D007378:Interleukins; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II
keywords: bladder pain syndrome; cytokine; inducible nitric oxide synthase; inflammatory mediators; interstitial cystitis; nitric oxide