Cytokine Expression in Patients with Bladder Pain Syndrome/Interstitial Cystitis ESSIC Type 3C

• Published in: The Journal of urology Vol. 192; no. 5; pp. 1564 - 1568
• Main Authors: Logadottir, Yr, Delbro, Dick, Fall, Magnus, Gjertsson, Inger, Jirholt, Pernilla, Lindholm, Catharina, Peeker, Ralph
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.11.2014
• Subjects: Abdominal Pain - genetics; Abdominal Pain - metabolism; Abdominal Pain - pathology; Biopsy; Cystitis; Cystitis, Interstitial - genetics; Cystitis, Interstitial - metabolism; Cystitis, Interstitial - pathology; cytokines; Cytokines - biosynthesis; Cytokines - genetics; Follow-Up Studies; Gene Expression Regulation; Immunohistochemistry; interleukins; interstitial; Medicin; Medicine; Nephrology; Njurmedicin; pain; Real-Time Polymerase Chain Reaction; Retrospective Studies; RNA, Messenger - genetics; Syndrome; urinary bladder; Urinary Bladder - metabolism; Urinary Bladder - pathology; Urology; Urothelium - metabolism; Urothelium - pathology; NO; interferon-γ; BPS; ESSIC; IFN-γ; iNOS; TGF-β; cytokines; IC; cystitis; interleukin; interstitial cystitis; polymerase chain reaction; pain; nitric oxide; IL; urinary bladder; interstitial; interleukins; inducible NO synthase; TNF-α; transforming growth factor-β; tumor necrosis factor-α; European Society of Study of Interstitial Cystitis; bladder pain syndrome; PCR
• ISSN: 0022-5347; 1527-3792; 1527-3792
• DOI: 10.1016/j.juro.2014.04.099

Purpose Bladder wall nitric oxide production in patients with bladder pain syndrome type 3C is increased compared to undetectable nitric oxide in patients with nonHunner bladder pain syndrome and healthy controls. However, the underlying mechanism/s of the increased nitric oxide production is largely unknown. We compared mRNA expression of a select group of cytokines in patients with bladder pain syndrome/interstitial cystitis type 3C and in pain-free controls. Materials and Methods Cold cup biopsies from 7 patients with bladder pain syndrome type 3C and 6 healthy subjects were analyzed. mRNA expression of IL-4, 6, 10 and 17A, iNOS, TNF-α, TGF-β and IFN-γ was estimated by real-time polymerase chain reaction. IL-17 protein expression was determined by immunohistochemistry. Mast cells were labeled with tryptase to evaluate cell appearance and count. Results IL-6, 10 and 17A, and iNOS mRNA levels as well as the number of mast cells infiltrating the bladder mucosa were significantly increased in patients with bladder pain syndrome type 3C compared to healthy controls. TNF-α, TGF-β and IFN-γ mRNA levels were similar in patients and controls. IL-17A expression at the protein level was up-regulated and localized to inflammatory cells and urothelium in patients with bladder pain syndrome type 3C. Conclusions Patients with bladder pain syndrome/interstitial cystitis had increased mRNA levels of IL-17A, 10 and 6, and iNOS. IL-17A might be important in the inflammatory process. To our knowledge the increase in IL-17A is a novel finding that may have new treatment implications.