Urodynamic changes in a noble rat model for nonbacterial prostatic inflammation

Bernoulli, Jenni; Yatkin, Emrah; Talvitie, Eva-Maria; Santti, Risto; Streng, Tomi

doi:10.1002/pros.20567

Cited by 26 publications

(36 citation statements)

References 40 publications

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“…Even if it is called CP with the NBP model generally, the grade of prostatic inflammation changes with methods of creation. In fact, the grade of prostatic inflammation in their NBP model [4] is considered to have more severity compared with our model. Since, the bladder function in their NBP model is considered to have been influenced.…”

Section: Discussionmentioning

confidence: 97%

“…These results indicated the bladder function is not influenced in this NBP model. Interestingly, Bernoulli et al [4] reported that urodynamic changes which developed in association with glandular inflammation indicated abnormal bladder function, reflecting an incipient obstruction, using the noble rat model for NBP with the estradiol and testosterone 21-day releasing implants. Even if it is called CP with the NBP model generally, the grade of prostatic inflammation changes with methods of creation.…”

Section: Discussionmentioning

confidence: 99%

“…Although the many animal models presenting CP has been reported, there are few reports of those urodynamic change [4,5]. Bernoulli et al [4] used the noble rat model for nonbacterial prostatic inflammation (NBP) with the estradiol and testosterone 21-day releasing implants.…”

Section: Introductionmentioning

confidence: 99%

“…Bernoulli et al [4] used the noble rat model for nonbacterial prostatic inflammation (NBP) with the estradiol and testosterone 21-day releasing implants. They reported that urodynamic changes which developed in association with glandular inflammation indicated abnormal bladder function, reflecting an incipient obstruction.…”

Section: Introductionmentioning

confidence: 99%

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Bladder function in 17β-estradiol-induced nonbacterial prostatitis model in Wister rat

et al. 2013

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Objectives: To investigated the bladder function of nonbacterial prostatitis (NBP) rat model that was induced by the injection of 17-estradiol in castrated rats. Methods:Ten-month-old male Wistar rats were divided into 2 groups (sham vs NBP; each N=8). NBP model was experimentally induced by castration followed by daily subcutaneous injection of 17-estradiol for 30 days. On the 31st day after surgery, we investigated several parameters; (1) Voiding behavior, (2) Bladder blood flow, (3) Measurements of the prostate and bladder weight, the levels of proinflammatory cytokines (TNF- and CXCL1) in the prostate and bladder, (4) Bladder contractile responses to electrical field stimulation (EFS), carbachol, and KCl.Results: (1) Voiding behavior (average micturition volume, total urine volume and number of micturitions) and (2) bladder blood flow were not significantly different between sham and NBP group. (3) NBP led to a significant decrease in the prostatic weight and increase in proinflammatory cytokine levels in the prostate, while NBP did not cause a significant change in the bladder weight or proinflammatory cytokine levels in the bladder.(4) Bladder contractile forces in response to EFS, carbachol and KCl were not significantly different between sham and NBP group. Conclusions:The present study suggests that NBP did not cause a significant change in the levels of proinflammatory cytokines in the bladder, and the bladder function is not influenced in this NBP model. Matsumoto S, et al. Bladder function in rat NBP model -3 -

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Bladder function in 17β-estradiol-induced nonbacterial prostatitis model in Wister rat

et al. 2013

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“…16 Although two models of prostatitis have recently been developed, they are of limited utility: one is bacterial 17 while the other is rat-based and requires the administration of exogenous hormones. 18 As a result, both of these models preclude the ability to cross-breed with other types of genetically manipulated mice to delineate and study specific mechanisms. Consequently the imperative remains to develop new mouse models for the study of prostatitis.…”

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confidence: 99%

Increased Endogenous Estrogen Synthesis Leads to the Sequential Induction of Prostatic Inflammation (Prostatitis) and Prostatic Pre-Malignancy

Ellem

Wang

Poutanen

et al. 2009

The American Journal of Pathology

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Prostatitis causes substantial morbidity to men, through associated urinary symptoms, sexual dysfunction, and pelvic pain; however, 90% to 95% of cases have an unknown etiology. Inflammation is associated with the development of carcinoma, and, therefore, it is imperative to identify and study the causes of prostatitis to improve our understanding of this disease and its role in prostate cancer. As estrogens cause prostatic inflammation, here we characterize the murine prostatic phenotype induced by elevated endogenous estrogens due to aromatase overexpression (AROM؉). Early-life development of the AROM؉ prostate was normal; however, progressive changes culminated in chronic inflammation and pre-malignancy. The AROM؉ prostate was smaller at puberty compared with wild-type controls. Mast cell numbers were significantly increased at puberty and preceded chronic inflammation, which emerged by 40 weeks of age and was characterized by increased mast cell, macrophage, neutrophil, and T-lymphocyte numbers. The expression of key inflammatory mediators was also significantly altered, and premalignant prostatic intraepithelial neoplasia lesions emerged by 52 weeks of age. Taken together, these data link estrogens to prostatitis and premalignancy in the prostate, further implicating a role for estrogen in prostate cancer. These data also establish the AROM؉ mouse as a novel, non-bacterial model for the study of prostatitis. Prostatitis, an exceedingly common condition in the male population worldwide, has an incidence of ϳ9% and a prevalence of ϳ14%, and, unlike benign prostatic hyperplasia and prostate cancer (PCa), which are predominantly diseases of older men, prostatitis afflicts men of all ages. It is also the most common outpatient condition seen in men under 50 years of age and accounts for more clinical visits than either PCa and/or benign prostatic hyperplasia.1,2 At present our knowledge of prostatitis is lacking, with 90% to 95% of cases having an unknown etiology. This represents a significant problem, particularly as prostatitis has also been implicated in the development of PCa.3-5 Given the prevalence of prostatitis and this putative link to PCa, it is vitally important to identify the unknown causes of prostatitis.Several causes of prostatitis have been postulated, including hormonal variation or exposure, infection due to sexually transmitted disease, 6 dietary factors, and physical trauma from urine reflux. 7 However, of particular interest is an apparent link between estrogen and prostatic inflammation, 8 which has emerged mainly from the administration of pharmacological levels of exogenous estrogen to rodents.9 Additional data obtained from further rodent studies show that the prostate gland is particularly sensitive to estrogenic exposure during development in fetal and neonatal life; transient estrogen exposure before puberty results in inflammation later in life, well after the exposure has occurred.10,11 Several decades of research from various laboratories, including our own, has demonstrated that...

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Steroid hormone imbalance drives macrophage infiltration and Spp1/osteopontin⁺ foam cell differentiation in the prostate

Popovics

Skalitzky

Schroeder

et al. 2023

The Journal of Pathology

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Benign prostatic hyperplasia (BPH) occurs progressively with aging in men and drives deteriorating symptoms collectively known as lower urinary tract symptoms (LUTS). Age‐associated changes in circulating steroid hormones, and prostate inflammation have been postulated in the etiology of BPH/LUTS. The link between hormones and inflammation in the development of BPH/LUTS is conflicting because they may occur independently or as sequential steps in disease pathogenesis. This study aimed to decipher the prostatic immune landscape in a mouse model of lower urinary tract dysfunction (LUTD). Steroid hormone imbalance was generated by the surgical implantation of testosterone (T) and estradiol (E2) pellets into male C57BL/6J mice and gene expression analysis was performed on ventral prostates (VPs). These experiments identified an increase in the expression of macrophage markers and Spp1/osteopontin (OPN). Localization studies of OPN pinpointed that OPN+ macrophages travel to the prostate lumen and transition into lipid‐accumulating foam cells. We also observed a significant increase in the number of tissue macrophages in the VP which was prevented in OPN‐knockout (OPN‐KO) mice. In contrast, mast cells, but not macrophages, were significantly elevated in the dorsal prostate of T + E2‐treated mice which was diminished in OPN‐KO mice. Steroid hormone implantation progressively increased urinary frequency, which was ameliorated in OPN‐KO mice. Our study underscores the role of age‐associated steroid hormone imbalances as a mechanism of expanding the prostatic macrophage population, their luminal translocation, and foam cell differentiation. © 2023 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

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Urodynamic changes in a noble rat model for nonbacterial prostatic inflammation

Cited by 26 publications

References 40 publications

Bladder function in 17β-estradiol-induced nonbacterial prostatitis model in Wister rat

Bladder function in 17β-estradiol-induced nonbacterial prostatitis model in Wister rat

Increased Endogenous Estrogen Synthesis Leads to the Sequential Induction of Prostatic Inflammation (Prostatitis) and Prostatic Pre-Malignancy

Steroid hormone imbalance drives macrophage infiltration and Spp1/osteopontin⁺ foam cell differentiation in the prostate

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Urodynamic changes in a noble rat model for nonbacterial prostatic inflammation

Cited by 26 publications

References 40 publications

Bladder function in 17β-estradiol-induced nonbacterial prostatitis model in Wister rat

Bladder function in 17β-estradiol-induced nonbacterial prostatitis model in Wister rat

Increased Endogenous Estrogen Synthesis Leads to the Sequential Induction of Prostatic Inflammation (Prostatitis) and Prostatic Pre-Malignancy

Steroid hormone imbalance drives macrophage infiltration and Spp1/osteopontin+ foam cell differentiation in the prostate

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Steroid hormone imbalance drives macrophage infiltration and Spp1/osteopontin⁺ foam cell differentiation in the prostate