Bladder pain syndrome/interstitial cystitis ESSIC type 3C: High expression of inducible nitric oxide synthase in inflammatory cells

Abstract

Objective. Bladder pain syndrome/interstitial cystitis (BPS/IC) includes a heterogeneous collection of underlying pathological conditions. Compared to the classic IC with a Hunner lesion, now denominated ESSIC type 3C, the non-Hunner type of BPS/IC appears different in a number of respects. In a previous study, measuring luminal nitric oxide (NO) in the bladder of patients with BPS/IC, it was reported that all patients with ESSIC type 3C had high levels of NO. The aim of the present study was to investigate the source of inducible nitric oxide synthase (iNOS) and thereby the cellular origin of NO production via iNOS. Material and methods. Immunohistochemistry, with two different anti-iNOS antibodies, was used to study10 patients with BPS/IC ESSIC type 3C who expressed high levels of intraluminal NO. These results were compared with four patients with non-Hunner BPS/IC. To substantiate further the involvement of iNOS in this condition, the protein expression of nitrotyrosine, a marker for iNOS activation, was also assessed. Results. On routine histopathology, the tissues of type 3C patients exhibited inflammatory infiltrates of varying intensity. Strong immunoreactivity for both iNOS and nitrotyrosine was noted within the urothelium but also within the inflammatory infiltrates in the lamina propria of these subjects. Conclusions. The findings of a clearly detectable protein expression of iNOS in both the urothelium and the inflammatory infiltrates in bladder biopsies from patients with BPS/IC ESSIC type 3C suggest that the production of NO, in this entity, may occur in different tissue compartments.

Key Words::

• bladder pain syndrome
• iNOS
• interstitial cystitis
• nitric oxide.

Acknowledgements

This study was supported by Anna-Lisa and Bror Björnssons Research Foundation, Märtha and Gustaf Ågrens Research Foundation and Sahlgrenska University Hospital project number ALF 7582. Örebro University is gratefully acknowledged for financial support. We are indebted to Chief Engineer Ulric Pedersen for excellent microphotographs.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.