A uropathogenic <i>E. coli</i> UTI89 model of prostatic inflammation and collagen accumulation for use in studying aberrant collagen production in the prostate

Ruetten, Hannah; Sandhu, Jaskiran K; Mueller, Brian; Wang, Peiqing; Zhang, Helen L.; Wegner, Kyle A; Cadena, Mark; Sandhu, Simran; Abler, Lisa L.; Zhu, Jonathan J.; O’Driscoll, Chelsea A.; Chelgren, Britta; Wang, Zunyi; Shen, Tian; Barasch, Jonathan; Bjorling, Dale E.; Vezina, Chad M.

doi:10.1152/ajprenal.00431.2020

Cited by 12 publications

(24 citation statements)

References 53 publications

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“…group of mice is most likely to have prostate inflammation (Ruetten et al, 2021). Infected mice have a greater density of prostate-localized inflammatory cells (CD45 immunopositive) than controls at 7 days post-infection, the same day that VSAs were performed (p = 0.0357, Figure 2a).…”

Section: Resultsmentioning

confidence: 96%

“…We recently characterized a model of male mouse UTI involving intraurethral administration of E. coli UTI89 and obtained VSA endpoint data from that study (Ruetten et al, 2021). The infected mouse group shown here includes only those mice that had more than 10,000 colony forming units of E. coli UTI89 in free catch urine 24 h after infection, as this F I G U R E 1 BTBR.…”

Section: Resultsmentioning

confidence: 99%

“…This study uses VSA data from previously published studies (Liu et al, 2019;Ruetten et al, 2021;Wegner et al, 2018Wegner et al, , 2020. In all studies, experiments were conducted under approved Animal Care and Use Committee Protocols at the University of Wisconsin-Madison.…”

Section: Void Spot Assay and Micementioning

confidence: 99%

“…All standard variables included in the Void Whizzard output were used without alteration, including standard units for spot size (cm 2 ), and default binning of spot sizes. A summary of mice and experimental variables for this study is listed in Table 1, and a comprehensive description of the procedures for blood glucose testing, E. coli UTI89 infection and urine culture, and subcutaneous slow-release testosterone and 17-β-estradiol implantation are described elsewhere (Liu et al, 2019;Ruetten et al, 2021;Wegner et al, 2018Wegner et al, , 2020.…”

Section: Void Spot Assay and Micementioning

confidence: 99%

“…Alternative approaches focus on urinary physiology and include cystometry, uroflowmetry, contrast enhanced ultrasound, and others. These methods can identify voiding function differences between experimental groups (Bjorling et al, 2015;Keil et al, 2016;Liu et al, 2019;Ruetten et al, 2019Ruetten et al, , 2021Turco et al, 2020;Wegner et al, 2018Wegner et al, , 2020 but are not proven diagnostic assays. For example, it is currently not possible to apply, in a blinded fashion, a single voiding function assessment to a mouse and use the experimental outcomes to accurately predict the underlying disease etiology (e.g., diabetic diuresis, irritative voiding, obstructive voiding, neurogenic voiding, or other).…”

Section: Introductionmentioning

confidence: 99%

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A NEW approach for characterizing mouse urinary pathophysiologies

et al. 2021

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Section: Resultsmentioning

confidence: 96%

Section: Resultsmentioning

confidence: 99%

Section: Void Spot Assay and Micementioning

confidence: 99%

Section: Void Spot Assay and Micementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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A NEW approach for characterizing mouse urinary pathophysiologies

et al. 2021

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Histologic inflammation and collagen content are not positively correlated in human BPH

Schneider,

Serrell,

Grimes

et al. 2023

The Prostate

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IntroductionRecent clinical studies have implicated prostate inflammation and fibrosis in the development of bladder outlet obstruction and lower urinary tract symptoms (LUTS). Studies utilizing rodent models, including work in our laboratory, have shown prostate fibrosis to occur as a consequence of inflammation. However, the relationship between collagen content and inflammation in human tissue samples obtained from surgical treatment of benign prostatic hypererplasia (BPH)/LUTS has not to our knowledge been previously examined.MethodsProstate tissue specimens from 53 patients (ages 47−88, mean 65.1) treated by open simple prostatectomy or transurethral resection of the prostate for BPH/LUTS were stained to quantitatively assess prostate inflammation and collagen content. Patients with prostate cancer present in greater than 5% of the surgical specimen were excluded. Prostate volume was determined from pelvic CT scan obtained within 2 years of surgery.ResultsAnalysis of the data showed that inflammation was inversely correlated with collagen content (r = −0.28, p = 0.04). In men with prostates less than 75 cm3 inflammation increases and collagen content decreases with prostate volume (p = 0.002 and p = 0.03, respectively) while in men with prostate volume over 75 cm3 inflammation decreases and collagen content increases with prostate volume (p = 0.30 and p = 0.005, respectively).ConclusionsOur data do not support the assumed positive association of prostate inflammation with collagen content. Coordinated analysis of scatter plots of inflammation and collagen content with prostate volume revealed a subset of prostates with volumes >50 cm3 prostate characterized by intense inflammation and low collagen content and it is this subgroup that appears most responsible for the inverse correlation of inflammation and collagen.

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Osteopontin deficiency leads to the resolution of prostatic fibrosis and inflammation

Popovics

Jain

Skalitzky

et al. 2021

Preprint

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Fibrogenic and inflammatory processes in the prostate are linked to the development of lower urinary tract symptoms (LUTS) in men. Our previous studies identified that osteopontin (OPN), a pro-fibrotic cytokine, is abundant in the prostate of men with LUTS and its secretion is stimulated by inflammatory cytokines potentially to drive fibrosis. This study investigates whether the lack of OPN ameliorates inflammation and fibrosis in the mouse prostate. We instilled uropathogenic E. coli (UTI89) or saline (control) transurethrally to C57BL/6J (WT) or Spp1tm1Blh/J (OPN-KO) mice and collected the prostates one or 8 weeks later. We found that OPN mRNA and protein expression were significantly induced by E. coli-instillation in the dorsal prostate (DP) after one week in WT mice. Deficiency in OPN expression led to decreased inflammation and fibrosis and the prevention of urinary dysfunction after 8 weeks. RNAseq analysis identified that E. coli-instilled WT mice expressed increased levels of inflammatory and fibrotic marker RNAs compared to OPN-KO mice including Col3a1, Dpt, Lum and Mmp3 which were confirmed by RNAscope. Our results indicate that OPN is induced by inflammation and prolongs the inflammatory state; genetic blockade of OPN accelerates recovery after inflammation, including a resolution of prostate fibrosis.

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A uropathogenic E. coli UTI89 model of prostatic inflammation and collagen accumulation for use in studying aberrant collagen production in the prostate

Cited by 12 publications

References 53 publications

A NEW approach for characterizing mouse urinary pathophysiologies

A NEW approach for characterizing mouse urinary pathophysiologies

Histologic inflammation and collagen content are not positively correlated in human BPH

Osteopontin deficiency leads to the resolution of prostatic fibrosis and inflammation

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