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The location of inflammation in the prostate might be an important factor affecting the severity of LUTS, especially voiding dysfunction.

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METHODS: Male SD rats at 8 weeks old were used. Prostatic inflammation was induced by 5% formalin injection into ventral lobes of the prostate and saline was injected in the control group (Sham). Rats with prostatic inflammation were divided into COX-2 inhibitor (celecoxib) therapy (Treatment) and placebo groups (Placebo). Rats were treated with celecoxib at a dose of 10mg/kg daily from 2 days before induction of prostatic inflammation. Twenty-eight days later, conscious cystometry was performed to assess bladder function. After cystometry, the prostate and L6-S1 dorsal root ganglia (DRG) were excised for analysis of mRNA expression levels of IL1b and COX-2 in the prostate and a Kþ channel a-subunit, Kv1.4, in DRG as well as histological evaluation of prostate and bladder.RESULTS: In cystometry, intercontraction intervals (ICI) were significantly decreased in Placebo group compared to Sham group. mRNA expressions of IL1b and COX-2 in the prostate were significantly increased while mRNA expression of Kv1.4 in L6-S1 DRG was significantly decreased in Placebo group compared to Sham rats. However, these changes were normalized in Treatment group. Prostatic sections from Placebo group demonstrated infiltration of inflammatory cells, but not in Sham or Treatment group. There were no significant inflammatory changes in bladder sections from any groups.CONCLUSIONS: COX-2 inhibition improved not only prostatic inflammation evidenced by decreases of upregulated IL1b and COX-2 levels, but also bladder overactivity as shown by shorter ICI in association with decreased Kv1.4 expression in pelvic afferent pathways. These results suggest that prostatic inflammation mediated by COX-2 plays an important role in bladder overactivity possibly induced by prostate-to-bladder cross-talk through pelvic afferent pathways. Thus, these COX-2-dependent mechanisms might contribute to male LUTS due to BPH associated with prostatic inflammation.

Aim Chronic prostatic inflammation is a critical factor that exacerbates lower urinary tract symptoms (LUTS). The serum C‐reactive protein (CRP) level is one of the most common markers with which to assess the degree of inflammation, and it has been reported to be related to the severity of LUTS. However, it is not clear whether the CRP level is linked to the magnitude of prostatic inflammation. We evaluated the relationship between the serum CRP level and the magnitude of prostatic inflammation and assessed the influence of CRP on the severity of LUTS. Methods We evaluated the tissue specimens of 121 benign prostatic hyperplasia (BPH) patients who underwent surgery for BPH and preoperative measurement of the serum CRP level. We quantified the magnitude of prostatic inflammation histologically by determining the number of high endothelial venule (HEV)‐like vessels and assessed the relationship between the serum CRP level and the HEV‐like vessels. We divided the patients into two groups based on the median serum CRP level and compared the clinical parameters of the two groups. Results The serum CRP level was correlated with the overactive bladder symptom score, whereas it was not correlated with the number of HEV‐like vessels. In filling cystometry and pressure‐flow study, the proportion of patients with detrusor overactivity in the higher‐CRP group was higher than that in the lower‐CRP group. Conclusions Our present study showed that the serum CRP level was significantly associated with storage dysfunction; in contrast, it was not a surrogate marker of prostatic inflammation.