The role of the prostatic stroma in chronic prostatitis/chronic pelvic pain syndrome

Dellabella, Marco; Milanese, Giulio; Sigala, Sandra; d'Anzeo, Gianluca; Arrighi, Nicola; Bodei, Serena; Muzzonigro, Giovanni

doi:10.1007/s00011-009-0086-7

Cited by 14 publications

(8 citation statements)

References 56 publications

(66 reference statements)

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“…Asymptomatic inflammatory . Type III chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS), accounts for approximately 90% of prostatitis diagnoses, and was formerly known as chronic nonbacterial prostatitis . Atypical microorganisms have been identified as causative organisms of chronic prostatitis.…”

Section: Discussionmentioning

confidence: 99%

“…26 Type III chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS), accounts for approximately 90% of prostatitis diagnoses, and was formerly known as chronic nonbacterial prostatitis. 27 Atypical microorganisms have been identified as causative organisms of chronic prostatitis. T. vaginalis and Chlamydia trachomatis are frequent causative pathogens, 28 and T. vaginalis has been reported in 1% to 17% of patients with NGU.…”

Section: Infiltration and Degranulation Of Mast Cells In The Prostamentioning

confidence: 99%

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Experimental rat prostatitis caused by Trichomonas vaginalis infection

et al. 2018

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Background Trichomonas vaginalis (T. vaginalis) is the most common sexually transmitted parasite. It has been detected in prostatic tissue of patients with prostatitis and reported to be associated with chronic prostatitis and benign prostatic hyperplasia as well as prostate cancer. Recently, experimental rodent models of prostatitis induced by pathogen infection have been developed. However, there have so far been no reports of prostatitis caused by T. vaginalis infection in animals. Here, we investigated whether infection with T. vaginalis via the rat urethra could cause prostatitis. Methods T. vaginalis was injected into prostate through urethra of rat (Wistar rats), and the rats were killed 1, 2, or 4 weeks later. The presence of T. vaginalis trophozoites in the rat prostates was examined by immunohistochemistry, and pathological changes of the prostate were observed by hematoxylin‐eosin staining and evaluated by grading from 0 to 5 for inflammatory cell infiltration, acinar changes, and interstitial fibrosis. Infiltrated mast cells were observed by toluidine blue staining of rat prostate tissue. Chemokine C‐C motif ligand 2 (CCL2) levels of the rat prostates were measured by ELISA. Results T. vaginalis trophozoites were observed in acini in the prostates of the injected rats. The prostate tissues had higher pathological scores, and 83% (5/6) and 100% (6/6) of the ventral and dorsolateral lobes (n = 6), respectively, were inflamed. Infiltration and degranulation of mast cells were observed at higher rates in prostate sections of the T. vaginalis‐infected rats. Also, prostate tissues of the injected rats had increased CCL2 levels. Conclusions Injection of T. vaginalis in rats caused prostatitis as revealed by pathologic changes, mast cell infiltration and increased CCL2 production. Therefore, this study provides the first evidence that T. vaginalis infection in rats causes prostatitis.

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Section: Discussionmentioning

confidence: 99%

Section: Infiltration and Degranulation Of Mast Cells In The Prostamentioning

confidence: 99%

Experimental rat prostatitis caused by Trichomonas vaginalis infection

et al. 2018

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“…The pSMC phenotypic changes are critical not only because they promote and sustain inflammation, but also because they alter stromal–epithelial interactions (Taboga et al, 2008). As a result, pSMCs have a protagonist role in the development, maintenance, and/or progression of prostatic diseases including prostatitis (Dellabella et al, 2009; Quintar et al, 2010), benign prostate hyperplasia (BPH), (Schauer and Rowley, 2011) and prostate cancer (Tuxhorn et al, 2001; Wong and Tam, 2002; Cunha et al, 2003). For instance, it has been reported that human stromal BPH cells express TLRs for different pathogens and actively contribute to chronic inflammation and prostatic hyperplasia by secreting proinflammatory cytokines and chemokines in response to TLR agonists (Penna et al, 2009).…”

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confidence: 99%

Testosterone abrogates TLR4 activation in prostate smooth muscle cells contributing to the preservation of a differentiated phenotype

Leimgruber

Quintar

García

et al. 2013

Journal Cellular Physiology

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Prostate smooth muscle cells (pSMCs) are capable of responding to inflammatory stimuli by secreting proinflammatory products, which causes pSMCs to undergo dedifferentiation. Although it has been proposed that androgens decrease proinflammatory molecules in many cells and under various conditions, the role of testosterone in the prostate inflammatory microenvironment is still unclear. Therefore, our aim was to evaluate if testosterone was able to modulate the pSMCs response to bacterial LPS by stimulating primary pSMC cultures, containing testosterone or vehicle, with LPS (1 or 10 µg/ml) for 24-48 h. The LPS challenge induced pSMCs dedifferentiation as evidenced by a decrease of calponin and alpha smooth muscle actin along with an increase of vimentin in a dose-dependent manner, whereas testosterone abrogated these alterations. Additionally, an ultrastructural analysis showed that pSMCs acquired a secretory profile after LPS and developed proteinopoietic organelles, while pSMCs preincubated with testosterone maintained a more differentiated phenotype. Testosterone downregulated the expression of surface TLR4 in control cells and inhibited any increase after LPS treatment. Moreover, testosterone prevented IκB-α degradation and the LPS-induced NF-κB nuclear translocation. Testosterone also decreased TNF-α and IL6 production by pSMCs after LPS as quantified by ELISA. Finally, we observed that testosterone inhibited the induction of pSMCs proliferation incited by LPS. Taken together, these results indicate that testosterone reduced the proinflammatory pSMCs response to LPS, with these cells being less reactive in the presence of androgens. In this context, testosterone might have a homeostatic role by contributing to preserve a contractile phenotype on pSMCs under inflammatory conditions.

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“…On digital rectal examination the prostate may be tender. During palpation patients may have tenderness of the pelvic floor muscles and a tight anal sphincter (Dellabella et al, 2009). …”

Section: Clinical Featuresmentioning

confidence: 99%