Chronic prostatic inflammation can lead to overactive bladder symptoms, such as bladder overactivity and persistent bladder discomfort/pain, causing substantial suffering and decreased quality of life in patients. However, the pathogenesis of chronic prostatitis is complex, and the mechanism of related bladder symptoms is not well understood. To date, few studies have considered the influence of psychological factors on chronic prostatitis (PRO) models. Here, we aim to refine a murine chronic prostatitis model combining chemically induced prostatitis with psychological stress to better simulate the possible pathogenesis in clinical practice and explore the effect of psychological stress on prostatitis and bladder function.

A total of 40 mice were randomly divided into four groups: normal control (NC) group, PRO group, water avoidance stress (WAS) group and PRO+WAS group. Ten mice were assigned to each group: five for cystometrography (CMG) and five for von Frey testing and histological analysis. PRO was induced through a prostatic injection of 10% paraformaldehyde (PFA). The WAS mice were placed on the middle platform for 1 hour per day for ten consecutive days.

The CMG results suggested that the PRO group, the WAS group and the PRO+WAS group all exhibited bladder overactivity, presented as a shortened micturition interval and decreased threshold pressure evoking bladder contraction (Figure 1). The symptoms of the PRO group and the PRO+WAS group were more severe than those of the WAS group. The tissue staining results indicated that WAS itself caused only mild prostatic inflammation but could significantly aggravate chemical-induced prostatic inflammation, as well as the total number of mast cells and proportion of activated mast cells. The results of the von Frey test demonstrated that both WAS and PRO induced bladder hyperalgesia in mice, and the WAS+PRO group showed significant pelvic pain symptoms either (Figure 2).

In the current study, we first established a refined murine model combining chemically induced prostatitis with psychological stress, and the model mice presented significant overactive bladder (OAB) symptoms and pelvic pain. In addition, the WAS+PRO model mice showed more severe prostatic inflammation than the PRO model mice and the WAS model mice, suggesting that WAS could aggravate prostatic inflammation and related symptoms. These results demonstrate that our innovative model can simulate the clinical situation well and is expected to be a reliable tool for basic research on chronic prostatitis.

Our refined murine PRO model could manifest persistent bladder overactivity, pelvic hyperalgesia and prostatic inflammation. WAS could induce mild prostatic inflammation and aggravate primary prostatic inflammation.

Continence 12S (2024) 101435
DOI: 10.1016/j.cont.2024.101435