Interstitial cystitis (IC)/chronic pelvic pain syndrome (CPPS) is a clinical syndrome of pelvic pain and/or urinary urgency/frequency in absence of a specific cause such as bacterial infection or damage to the bladder. The pathogenetic mechanisms of IC/CPPS are as yet undefined and it is largely this lack of knowledge, which precludes a systematic therapeutic approach. Experimental evidence, including results from the animal models of cystitis and the knock-out mice, indicate a participation of tachykinin receptors, especially the NK1R, in neurogenic inflammation, which is considered an important element of the IC complex. However, there is very scant information about the molecular mechanisms of IC in humans, or of the types of receptors, which participate in neurogenic inflammation. Based on our molecular biological know-how and the clinical expertise, we propose to investigate the role of the tachykinin and bradykinin receptors and their signalling partners in CPPS and bladder dysfunction in humans.
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Receptor expression in disease states versus control
Timeframe: at time of biospy