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The exact pathophysiology of interstitial cystitis/painful bladder syndrome is unknown; however, autoimmunity is a valid theory. We developed an autoimmune chronic cystitis model by administration of the medium dose of immunogenic peptide T2. Sixty female C57BL/6 mice were divided into six groups. The control group was not treated with any reagent. CFA group was injected with CFA + normal saline, homogenate group with bladder homogenate + CFA, low-dose group with low dose of T2 peptide + CFA, medium dose group with the medium dose of T2 peptide + CFA, and high-dose group with the high dose of T2 peptide + CFA. Micturition habits, withdrawal frequencies of mice, and bladders weight were measured for each group. Hematoxylin and eosin staining and toluidine blue staining were used to investigate bladder inflammation and mast cells accumulation, respectively. T cells infiltration in the bladder tissues and serum TNF-α level were measured by using immunohistochemistry and ELISA, respectively. Mice immunized with the medium dose of T2 peptide (0.225 mg/ml) were extremely sensitive to the applied force, showed greater urine frequencies, and higher bladder weights. Histologic examination revealed severe edema and inflammation in bladder tissues of medium-dose group. Extensive infiltration of T cells in bladder tissues, elevated TNF-α, and increased mast cells accumulation were observed in medium-dose group as compared to that in other groups. EAC mice model established by injecting the medium dose of T2 (0.225 mg/ml) mimics all the symptoms and pathophysiologic characteristics of IC/PBS. We believe that this model can help us to investigate the pathogenesis of IC/PBS.

A mouse model was developed to simulate the clinical features of chronic prostatitis/chronic pelvic pain syndrome using peptide (T ). Forty C57BL/6 mice were divided into four groups of 10 mice each, averagely and randomly. T plus aluminium hydroxide adjuvant group was given subcutaneous injection with the emulsion mixture of T and aluminium hydroxide adjuvant, the T group with T , the aluminium hydroxide adjuvant group with aluminium hydroxide adjuvant and the normal control group with 0.9/% NaCl solution. Haematoxylin andeosin staining was used to observe the inflammation of the prostate. Plasma levels of TNF-α and CRP were detected by ELISA kit. The expression of IL-1βin the prostate was investigated by immunohistochemistry. The statistical differences between the groups were compared by t test. Histopathological analyses demonstrated that prostate lesions were most severe in the group immunised with T plus aluminium hydroxide adjuvant. Plasma levels of TNF-α and CRP were statistically elevated compared with control groups. The expression levels of IL-1β in the prostate were more obvious than control groups. T in aluminium hydroxide adjuvant subcutaneous injection could successfully set up experimental autoimmune prostatitis in C57BL/6 mice. This murine model would be greatly beneficial to further comprehend the aetiology, pathogenesis and explicit treatment of CP/CPPS.

Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a complex disease of unclear etiology. Precise treatment of CP/CPPS is not available due to lack of specific cause; however, autoimmunity is the most valid theory. We develop a new treatment strategy that involves synthesis and coupling of biodegradable nanoparticles to antigenic T2 peptide to induce immune tolerance in CP/CPPS mice models. A total of 50 male C57BL/6 mice were randomized into five groups, that is, naïve, Model, PLGA‐PEMA, PLGA‐PEMA‐OVA323‐339, and PLGA‐PEMA‐T2 group. All groups except naïve were injected subcutaneously on day 0 with 0.2 mL of T2 peptide with CFA to generate valid CP/CPPS models. After successful induction of CP/CPPS, Model group, PLGA‐PEMA, PLGA‐PEMA‐OVA, and PLGA‐PEMA‐T2 groups were treated with 0.15 mL of normal saline, 0.2 mg of PLGA‐PEMA and PLG‐PEMA‐T2 and 0.3 mg PLGA‐PEMA‐OVA nanoparticles, respectively, on day 28. Hematoxylin and eosin staining, and ELISA were used to evaluate the variation in CP/CPPS manifestations and seral level of IL‐10 in each group. Pain threshold and voiding behavior were also recorded for every group. Mice treated with PLGA‐PEMA‐T2 exhibited enhanced pain threshold, reduced urine frequency, and prostate pathology. Furthermore, serum level of inflammatory mediators (TNF‐α and CRP) were reduced and anti‐inflammatory IL‐10 was enhanced in PLGA‐PEMA‐T2 group as compared to other groups. Our results demonstrate that PLGA‐PEMA‐T2 nanoparticle ameliorates disease manifestations in CP/CPPS mice models and upregulates IL‐10 which is essential for tolerance induction. This strategy highlights the new therapeutic approach utilizing biodegradable nanoparticles for the treatment of CP/CPPS.