Inflammation In Benign Prostatic Hyperplasia Research Articles

Correlation of Total Serum Prostate Specific Antigen and Prostate Specific Antigen Density with subclinical inflammation in Benign Prostatic Hyperplasia

Background Serum PSA is an important tumor marker for diagnosis of prostate cancer. However, it can rise in some other benign conditions like benign prostatic hyperplasia (BPH), prostatitis, prostatic infarct, instrumentation, prostate manipulations like examination, transurethral resection and urinary tract infection (UTI). The aim of this study was to find correlation of total serum PSA and PSAD with extent and aggressiveness of subclinical inflammation in BPH.MethodsThis cross-sectional study was conducted on 25 cases of transurethral resection of prostate and open prostatectomy specimens diagnosed with BPH received in time period of July 2022 to June 2023. Cases with clinical signs and symptoms of prostatitis, positive urine culture, diagnosed as prostate cancer, cases with history of previous surgery of prostate and history of instrumentation of urinary tract were excluded. Total serum PSA and prostate weight were measured. PSAD was calculated. Histological inflammation was graded with respect to extent and aggressiveness. PSA and PSAD were correlated with extent and aggressiveness of inflammation.ResultsThere was no statistically significant correlation between inflammation extent score and total serum PSA (p = 0.318). Also, there was no correlation between inflammation extent score and PSAD (p = 0.308). However, there was significant correlation between inflammation aggressiveness score and total serum PSA (p = 0.011). Similarly, there was also correlation between inflammation aggressiveness score and PSAD (p = 0.010).Conclusions Repeat unnecessary biopsies may be avoided in cases with high total serum PSA in presence of glandular epithelial disruption in histological prostatitis.

Benign Prostatic Hyperplasia (BPH): A Comprehensive Analysis of the Malaise and Summarizing Possible Management Options through Phytotherapeutic Agents

Benign prostatic hyperplasia (BPH) is a severe illness affecting middle-aged and geriatric male patients. This disease normally occurs at the age of 40 or above and is also associated with sexual dysfunction. Alpha-blockers and 5α-reductase inhibitors are the preferred drugs practiced to treat BPH. However, invasive surgical therapy remains the gold standard for managing the condition in the case of refractory and intricate BPH conditions. Due to the fear of sexual dysfunction and the detrimental influence on their quality of life, most patients seek to avoid synthetic drugs and surgery. For this reason, several patients turn to phytotherapy and other alternative therapies. The authors looked at the existing perceptions of epidemiology, etiology, and pathophysiology associated with BPH in this review article. In addition, this article contained basic information on the pathological roles of inflammation in BPH and various diagnoses and treatment options. It was well reported that the administration of medicinal herbs played a vital role in managing BPH. In recent years, many researchers worldwide have reported the efficiency and safety of phytochemicals in managing numerous pathological disorders in-vivo and in-vitro conditions and the prevention of illness.

Relationship of interleukin‐23 with matrix metalloproteinase‐9, pentraxin‐3, sleep quality and prostate size in benign prostatic hyperplasia

Benign prostatic hyperplasia (BPH) is known to be associated with sleep disturbance and inflammation. The objective of the study was to assess the levels of serum MMP-9 and its inhibitor (TIMP-1), interleukin-23 and pentraxin-3 and their association with sleep quality index and prostate size in BPH patients. Eighty-eight BPH patients were recruited based on clinical and ultrasound findings. MMP-9 and its inhibitor (TIMP-1), interleukin-23 and pentraxin-3 were estimated in all the subjects. Sleep quality was assessed using Pittsburgh Sleep Quality Index (PQSI). Interleukin-23 was significantly correlated with prostate size (p=0.031), TIMP-1 (p=0.035), MMP-9 (p=0.004) and PSQI score (p=0.020). TIMP-1 was significantly correlated with MMP-9 (p=0.006) and prostate size (p=0.016). Pentraxin-3 was positively correlated with PSQI score (p=0.047). Multivariate analysis shows that interleukin -23 (p=0.006) predicts prostate enlargement in BPH patients. Interleukin-23 was significantly increased in BPH patients with PSQI score >9 compared to those with PSQI <9. We conclude that poor sleep quality contributes to inflammation in BPH. Inflammation leads to prostate enlargement in patients with BPH.

Epigallokateşin-3-gallat'ın benign prostat hiperplazi hücrelerinde migrasyon ve enflamasyon ile ilişkili genlerin transkripsiyonel regülasyonuna etkisi

Objective: This study was aimed to evaluate the role of epigallocatechin-3-gallate (EGCG) in the transcriptional regulation of genes associated with migration and inflammation in benign prostate hyperplasia (BPH-1) cells.&#x0D; Material and Methods: Effect of EGCG treatment on expressions of FAK, PXN, RhoA, Rac1, Cdc42, PAK1, ROCK1, WASL genes related to migration and IL-8, IL-6, NFκB p50, NFκB p65, IκBα genes related to inflammation were determined by quantitative real time-polymerase chain reaction (qRT-PCR).&#x0D; Results: It was determined that EGCG treatment did not significantly change the expressions of investigated genes over 2 fold in terms of mRNA levels. EGCG, which effectively suppresses protein phosphorylations and levels, does not play a role in transcriptional regulation of migration and inflammation-related genes. These results show that EGCG probably reduces the activity of FAK and NFκB signaling pathways by altering the protein function without affecting mRNA levels. &#x0D; Conclusion: It is thought that EGCG may be useful in the treatment of premalignant lesions such as LUTS (lower urinary tract symptoms) and BPH, and its mechanism of action can be predominantly realized at post-translational level.

Effects of Saussurea costus on apoptosis imbalance and inflammation in benign prostatic hyperplasia

Ethnopharmacological relevanceSaussurea costus (synonym: Aucklandia lappa Decne) is a medicinal plant distributed in Yunnan, Guangxi, and Sichuan in China. In traditional Korean medicine, the plant parts (especially the root—“radix aucklandiae”) is widely used to treat vomiting, diarrhea, and inflammation. However, little has been reported on its effect on benign prostatic hyperplasia (BPH), which is common in middle-aged men. Aim of the studyBPH is caused by apoptosis imbalance and inflammation due to aging of the prostate. Therefore, the aim of this was to prove the efficacy of S. costus by analyzing its effect on the biological mechanisms leading to BPH progression. Materials and methodsWistar rats were injected subcutaneously with a single dose of testosterone (125 mg/kg) to induce BPH, and were later administered with S. costus (20, 40 mg/kg). After 12 weeks, histological changes in the prostate and hormone regulation factors were assessed in all animals. Furthermore, apoptotic protein and apoptotic body values were analyzed to confirm the improvement of apoptosis imbalance, and inflammatory cytokines were analyzed to confirm the anti-inflammatory efficacy of S. costus. ResultsIn the serum and tissue of S. costus-treated BPH rats, a significant reduction in prostate weight, prostate index, and hormone regulation factors was observed. S. costus also increased the levels of apoptosis marker proteins and reduced the levels of inflammatory cytokines. It also decreased the expression of B-cell lymphoma 2 (BCL-2) and increased the expression of BCL-2 associated X protein (BAX) in the prostate. Histological changes such as epithelial thickness significantly increased in BPH induced group but significantly decreased in the S. costus-treated groups (p < 0.001). ConclusionsS. costus may prevent and treat BPH occurrence by modulating inflammation and apoptosis imbalance.

Pharmacological Effects and Potential Clinical Usefulness of Polyphenols in Benign Prostatic Hyperplasia.

Benign prostatic hyperplasia (BPH) is arguably the most common benign disease among men. This disease is often associated with lower urinary tract symptoms (LUTS) in men and significantly decreases the quality of life. Polyphenol consumption reportedly plays an important role in the prevention of many diseases, including BPH. In recent years, in addition to disease prevention, many studies have reported the efficacy and safety of polyphenol treatment against various pathological conditions in vivo and in vitro. Furthermore, numerous studies have also revealed the molecular mechanisms of the antioxidant and anti-inflammatory effects of polyphenols. We believe that an improved understanding of the detailed pharmacological roles of polyphenol-induced activities at a molecular level is important for the prevention and treatment of BPH. Polyphenols are composed of many members, and their biological roles differ. In this review, we first provide information regarding the pathological roles of oxidative stress and inflammation in BPH. Next, the antioxidant and anti-inflammatory effects of polyphenols, including those of flavonoids and non-flavonoids, are discussed. Finally, we talk about the results and limitations of previous clinical trials that have used polyphenols in BPH, with particular focus on their molecular mechanisms of action.

Review of the Roles and Interaction of Androgen and Inflammation in Benign Prostatic Hyperplasia.

The lower urinary tract symptoms (LUTSs) and acute urinary retention (AUR) caused by benign prostatic hyperplasia (BPH) can seriously affect the quality of life of elderly men. Studies suggest that both androgens and inflammation greatly influence the occurrence and development of BPH in most patients. These two factors combined can also affect each other, leading to pathological changes in the stromal and epithelial tissue of the prostate transition zone in BPH patients. DHT in the prostate tissue of BPH patients may activate a chronic inflammatory response in the prostate, amplifying the expression of inflammatory factors and upregulating the proliferation ability of prostate tissue.

INFLAMMATION CHRONIQUE ET HYPERPLASIE BÉNIGNE DE LA PROSTATE: FACTEURS PRÉDICTIFS ET CONSÉQUENCES APRÈS CHIRURGIE OUVERTE CHRONIC INFLAMMATION AND BENIGN PROSTATIC HYPERPLASIA: PREDICTIVE FACTORS AND CONSEQUENCES AFTER OPEN SURGERY

Background: Chronic inflammation of the prostate has been observed on prostatic specimen after resection or a biopsy. The aim of this study was to determine the factors that can predict its existence in benign prostatic hyperplasia (BPH) and the consequences after open surgery. Method: We carried out a retrospective, observational, transversal study of patients who underwent prostatic adenomectomy in 2017 and 2018 in our department. Specimen with prostatic adenocarcinoma were excluded. &#x0D; Results: Of 51 operated patients, 31 (60.78%) had chronic inflammation within BPH. The mean delay between the beginning of symptoms and the surgery was 23.14 ± 35.62 months. &#x0D; Acute urinary retention was the main reason for consultation (78.43%). The mean duration of bladder catheter wear before surgery was 82.41 ± 220.36 months. Postoperative course was uneventful in 26(50.99%) patients. The mean postoperative stay was 5.86 ± 3.42 days. Surgical treatment delay (p = 0.000001), surgical wound infection (p = 0.002) and the length of postoperative stay (p = 0.002) had a significant correlation with prostatic chronic inflammation. &#x0D; Conclusion: The delay in surgical management was the main predictor of chronic inflammation in BPH. This factor increase the risk of surgical wound infection and an extended of postoperative stay.

In Silico and In Vitro Study: COX-2 Inhibition by Ethanol Extract of Dayak Onion Bulb (Eleutherine Americana Merr) as Treatment Innovation of Benign Prostatic Hyperplasia (BPH).

Benign Prostatic Hyperplasia (BPH) is a benign tumor in males, which is histopathologically known with an increase of epithelial cells and prostatic stroma. Androgens, estrogens, stroma-epithelial interactions, growth factors, and chronic inflammation play a key role in the occurrence of BPH. Chronic inflammation in BPH is characterized by excessive expression of COX-2, which will trigger the expression of Bcl-2 anti-apoptotic protein. Dayak onion (Eleutherine Americana Merr) is a typical Kalimantan plant that is known as the treatment for prostate disease. This plant contains flavonoids which can inhibit the COX-2 enzyme thus causing a reduction in the production of prostaglandin E2. This research was experimental research computationally and in vitro laboratory experimental research to determine COX-2 inhibitory activity by ethanol extracts of Dayak onion. In in silico flavonoid, it was strongly related to COX-2 receptor on the active side of TYR371. Thus, it had the potential to inhibit COX-2. COX-2 inhibitor would cause BCL-2 to be inactive so that apoptosis occurr in BPH. In the in vitro research using human whole blood assay, the Dayak Onion bulb ethanol extract had IC50 COX-2 of 40.57 ng/ml and IC50 COX-1 of 364.89 ng/ml. Therefore, the ratio of IC50 COX-2 to IC50 COX-1 was 0.11. Ethanol extract of Dayak onion bulb has an inhibitory activity against COX-2. Thus, it has a potential of being an innovation for BPH treatment. Patient Summary: A healthy male, age 25-35 years old (history taking, physical and laboratory examination), and not using NSAIDs for the past 2 weeks.

Inhibition of chronic prostate inflammation by hyaluronic acid through an immortalized human prostate stromal cell line model.

Benign prostatic hyperplasia (BPH) is the most common urologic disease among elderly men. A well-established in vitro cell model is required to determine the therapeutic mechanism of BPH inflammation. In this study, we attempted to establish an immortalized human prostate stromal cell line by transfecting with HPV-16 E6/E7 and designated as ihPSC. No significant difference was found in fibroblast-like morphology between primary hPSC and ihPSC. The ihPSC possessed a significantly higher cell proliferation rate than primary hPSC. The prostate-specific markers and proteins including cytoskeleton (α-SMA and vimentin) and smooth muscle (calponin), especially the androgen receptor (AR) were also examined in ihPSC, almost identical to the primary hPSC. To create an in vitro model featuring chronic prostatic inflammation, ihPSC was stimulated with IFN-γ+IL-17 and then treated with the high molecular weight hyaluronic acid hylan G-F 20 as an alternative strategy for inhibiting BPH inflammation. Hylan G-F 20 could dose-dependently diminish the inflammation-induced proliferation in ihPSC. The enhanced expressions of inflammatory molecules including IL-1β, IL-6, IL-8, cyclooxygenase 2 (COX2), inducible nitrogen oxide synthase (iNOS), and Toll-like receptor 4 (TLR4) were all abolished by hylan G-F 20. For inflammatory signaling, hylan G-F 20 can also diminish the IFN-γ+IL-17-increased expression of iNOS and p65 in ihPSC. These findings suggest that ihPSC could provide a mechanism-based platform for investigating prostate inflammation. The hylan G-F 20 showed strong anti-inflammatory effects by decreasing inflammatory cytokines and signalings in the ihPSC, indicating its therapeutic potentials in BPH treatment in the future.

Inflammasomes are important mediators of prostatic inflammation associated with BPH.

BackgroundThere is mounting evidence to support the role of inflammation in benign prostate hyperplasia (BPH), and a recent study reported expression of inflammasome derived cytokine IL-18 in prostate biopsy of BPH patients. Here we examined the expression of inflammasome-derived cytokines and activation of nucleotide-binding oligomerization domain-like receptor with pyrin domain protein 1 (NLRP) 1 inflammasome in a rat model of prostatic inflammation relevant to BPH.MethodsProstatic inflammation was experimentally induced in three-month-old male Sprague–Dawley rats by intraprostatic injection (50 μL) of either 5 % formalin or saline (sham) into the ventral lobes of prostate. 7 days later, prostate and bladder tissue was harvested for analysis of inflammasome by Western blot, immunohistochemistry and downstream cytokine production by Milliplex.ResultsExpression of interleukins, CXC and CC chemokines were elevated 2-15 fold in formalin injected prostate relative to sham. Significant expression of NLRP1 inflammasome components and caspase-1 in prostate were associated with significant elevation of pro and cleaved forms of IL-1β (25.50 ± 1.16 vs 3.05 ± 0.65 pg/mg of protein) and IL-18 (1646.15 ± 182.61 vs 304.67 ± 103.95 pg/mg of protein). Relative to prostate tissue, the cytokine expression in bladder tissue was much lower and did not involve inflammasome activation.ConclusionsSignificant upregulation of NLRP1, caspase-1 and downstream cytokines (IL-18 and IL-1β) suggests that a NLRP1 inflammasome is assembled and activated in prostate tissue of this rat model. Recapitulation of findings from human BPH specimens suggests that the inflammasome may perpetuate the inflammatory state associated with BPH. Further clarification of these pathways may offer innovative therapeutic targets for BPH-related inflammation.

Androgen receptor and immune inflammation in benign prostatic hyperplasia and prostate cancer

Both benign prostatic hyperplasia (BPH) and prostate cancer (PCa) are frequent diseases in middle-aged to elderly men worldwide. While both diseases are linked to abnormal growth of the prostate, the epidemiological and pathological features of these two prostate diseases are different. BPH nodules typically arise from the transitional zone, and, in contrast, PCa arises from the peripheral zone. Androgen deprivation therapy alone may not be sufficient to cure these two prostatic diseases due to its undesirable side effects. The alteration of androgen receptor-mediated inflammatory signals from infiltrating immune cells and prostate stromal/epithelial cells may play key roles in those unwanted events. Herein, this review will focus on the roles of androgen/androgen receptor signals in the inflammation-induced progression of BPH and PCa.

Stromal Response to Prostate Cancer: Nanotechnology-Based Detection of Thioredoxin-Interacting Protein Partners Distinguishes Prostate Cancer Associated Stroma from That of Benign Prostatic Hyperplasia

Histological staining of reactive stroma has been shown to be a predictor of biochemical recurrence in prostate cancer, however, molecular markers of the stromal response to prostate cancer have not yet been fully delineated. The objective of this study was to determine whether or not the stromal biomarkers detected with a thioredoxin-targeted nanodevice could be used to distinguish the stroma associated with benign prostatic hyperplasia from that associated with PCA. In this regard, we recently demonstrated that a thioredoxin-targeted nanodevice selectively binds to reactive stroma in frozen prostate tumor tissue sections. To accomplish this, random frozen prostate tissue sections from each of 35 patients who underwent resection were incubated with the nanodevice and graded for fluorescent intensity. An adjacent section from each case was stained with Hematoxylin & Eosin to confirm the diagnosis. Select cases were stained with Masson's Trichrome or immunohistochemically using antibodies to thioredoxin reductase 1, thioredoxin reductase 2 or peroxiredoxin 1. Our results demonstrate that the graded intensity of nanodevice binding to the stroma associated with PCA was significantly higher (p = 0.0127) than that of benign prostatic hyperplasia using the t-test. Immunohistochemical staining of adjacent sections in representative cases showed that none of the two commonly studied thioredoxin interacting protein partners mirrored the fluorescence pattern seen with the nanodevice. However, thioredoxin reductase 2 protein was clearly shown to be a biomarker of prostate cancer-associated reactive stroma whose presence distinguishes the stroma associated with benign prostatic hyperplasia from that associated with prostate cancer. We conclude that the signal detected by the nanodevice, in contrast to individual targets detected with antibodies used in this study, originates from multiple thioredoxin interacting protein partners that distinguish the M2 neutrophil and macrophage associated inflammatory response in prostate cancer-associated stroma from the CD4+ T-Lymphocyte linked inflammation in benign prostatic hyperplasia.

Correlation between benign prostatic hyperplasia and inflammation

This review aims to evaluate the available evidence on the role of prostatic inflammation in the pathogenesis and progression of benign prostatic hyperplasia (BPH). Although there is still no evidence of a causal relation, accumulating evidence suggests that inflammation may contribute to the development of BPH and lower urinary tract symptoms (LUTS). Inflammatory infiltrates are frequently observed in prostate tissue specimens from men with BPH and the presence or degree of inflammation has been found to be correlated with prostate volume and weight. The inflammatory injury may contribute to cytokine production by inflammatory cells driving local growth factor production and angiogenesis in the prostatic tissue. This proinflammatory microenvironment is closely related to BPH stromal hyperproliferation and tissue remodeling with a local hypoxia induced by increased oxygen demands by proliferating cells which supports chronic inflammation as a source of oxidative stress leading to tissue injury in infiltrating area. Although the pathogenesis of BPH is not yet fully understood and several mechanisms seem to be involved in the development and progression, recent studies strongly suggest that BPH is an immune inflammatory disease. The T-cell activity and associated autoimmune reaction seem to induce epithelial and stromal cell proliferation. Further understanding of the role of inflammation in BPH and clinical detection of this inflammation will expand the understanding of BPH pathogenesis and its histologic and clinical progression, allow risk stratification for patients presenting with BPH-related LUTS, and suggest novel treatment strategies.

The effect of prostate tissue inflammation in benign prostatic hyperplasia on enhancer of zeste homolog 2 ribonucleic acid expression

BACKGROUND AND OBJECTIVESEnhancer of zeste homolog 2 (EZH2) has been recently found to regulate several genes involved in immunoresponse and autocrine inflammation network. The aim of the study was to quantitate EZH2 messenger ribonucleic acid (mRNA) expression, evaluate its relation to conditions of prostatitis associated with benign prostatic hyperplasia (BPH), and correlate it with the levels of the inflammatory marker interlukin 6 (IL-6).DESIGN AND SETTINGCross-sectional study in Middle Eastern men with BPH and prostatitis or BPH only.PATIENTS AND METHODSTransrectal ultrasound–guided prostate biopsies were collected from 106 patients suspected of having prostate cancer; however, the histology revealed BPH. Upon further pathological examination, 56 of these cases were identified as BPH with prostatitis and classified as: acute prostatitis (n=13); active chronic prostatitis (n=32); and, chronic inactive prostatitis (n=12). Serum IL-6 levels and EZH2 mRNA expression were measured and compared between patient groups.RESULTSEZH2 mRNA was overexpressed in BPH with prostatitis patients compared to BPH only patients (P<.0001). BPH with active chronic prostatitis had higher EZH2 expression than BPH with acute or chronic inactive prostatitis compared to BPH only (P=.05 and .73, respectively). EZH2 mRNA expression showed a negative correlation with IL-6 concentrations in BPH with prostatitis patients (rs=−0.31, P=.02). EZH2 overexpression was associated with an increased risk of having BPH with prostatitis (crude odds ratio 0.20, 95% CI 0.06–0.65, P=.0076).CONCLUSIONSEZH2 mRNA expression correlates positively with prostatitis conditions associated with BPH and negatively with serum IL-6 levels. This supports the possible involvement of EZH2 mRNA overexpression in the development of prostate inflammation, and its new regulatory role in suppressing the expression of some inflammatory network genes.

111 Three key chemokines (CCL2, CXCL10 AND IL8) involved in benign prostatic hyperplasia inflammation are reduced by Permixon® treatment

111 Three key chemokines (CCL2, CXCL10 AND IL8) involved in benign prostatic hyperplasia inflammation are reduced by Permixon® treatment

Inflammation and Benign Prostatic Hyperplasia: Clinical Implications

Prostatic inflammation may be a large contributor to hyperplastic changes in the prostate. There have been several studies looking at the varieties of growth factors and cytokines that are involved in both the inflammatory process and in the epithelial/stromal prostatic cells interactions. We reviewed the recent international literature using a PubMed search to analyze new findings supporting a role for inflammation in benign prostatic hyperplasia (BPH) progression. This article reviews the factors that lead to both intrinsic and extrinsic causes of prostatic inflammation. There are several exciting studies supporting that inflammation can promote chronic prostatic diseases, such as BPH.

Biomarkers for the diagnosis of prostatic inflammation in benign prostatic hyperplasia

Chronic prostatic inflammation could be a central mechanism in benign prostatic hyperplasia (BPH) progression. Currently, the histological examination of prostate biopsies remains the only way to diagnose prostatic inflammation. Our objective was to find new noninvasive biomarkers for the diagnosis of prostatic inflammation. Ninety BPH samples were investigated in two steps. First, a hypothesis was generated using a profiling procedure with a panel of 96 genes on an initial set of 30 samples. Then, the candidate biomarkers were validated on a large number of samples (n = 90). Gene expression was compared with the histological prostatic inflammation score based on the density and the confluence of lymphoid nodules. Finally, protein transcripts of the candidate biomarkers were investigated in urine samples and compared with clinical data. Of the 96 genes, nine were significantly correlated with the inflammation score on the initial set of patients. Four of them were validated on the complete set of patients: CCR7, CD40LG, CTLA4, and ICOS. ICOS and CTLA4 protein levels were readily measured in urine samples using a conventional ELISA procedure. High-ICOS expression in urine was associated with a higher post-void residual and a lower maximum urinary flow rate. Four genes were significantly upregulated at the mRNA level in the prostate tissue of patients with severe inflammation score. Two proteins were measured in urine samples, and were associated with maximum uroflowmetry and post-void residual. A prospective clinical study is needed to confirm their clinical relevance.

Cyclooxygenase-2 Overexpression in Chronic Inflammation Associated with Benign Prostatic Hyperplasia: Is It Related to Apoptosis and Angiogenesis of Prostate Cancer?

PurposeThis study was performed to investigate the relationship between cyclooxygenase-2 (COX-2) expression and apoptosis/angiogenesis in inflammatory and noninflammatory benign prostatic hyperplasia (BPH) and prostate cancer (PC).Materials and MethodsThis study involved 64 BPH and 57 PC patients. The BPH histopathologies were classified by the presence of chronic inflammation as follows: noninflammatory BPH (NI-BPH; n=23) and inflammatory BPH (I-BPH; n=41). The association between the expression of COX-2, expression of Bcl-2, the apoptotic index (AI), expression of vascular endothelial growth factor (VEGF), and microvascular density (MVD) in the prostate was investigated.ResultsAn overexpression of COX-2, Bcl-2, and VEGF was observed in cases of PC compared with cases of BPH. In PC, the AI was lower and MVD was higher than in BPH. In NI-BPH, I-BPH, and PC, the overexpression of COX-2, Bcl-2, and VEGF gradually increased. The AI was high in I-BPH, but did not differ significantly between the NI-BPH and I-BPH groups or between the NI-BPH and PC groups. MVD was significantly high in PC, but no significant difference was found between NI-BPH and I-BPH. A significant correlation was shown between the overexpression of COX-2 and Bcl-2, and COX-2 and VEGF. However, the AI was not correlated with the overexpression of COX-2 or Bcl-2. MVD was correlated with the overexpression of COX-2 and VEGF.ConclusionsCOX-2 overexpression in PC is correlated with a decrease in apoptosis and an increase in angiogenesis. Chronic inflammation in BPH causes an overexpression of COX-2, which induces the increased expression of Bcl-2 and VEGF. It is likely that chronic inflammation plays a role in the intermediate step of carcinogenesis in the prostate.

Inflammation et hyperplasie bénigne de la prostate : cause ou conséquence ?

Although benign prostatic hyperplasia (BPH) is the most frequent disease in elderly men, only a few predictive factors have been clearly identified. Recently, chronic prostatic inflammation has emerged as one of them. This review aims at describing the scientific proof of a relationship between chronic prostatic inflammation and BPH. Searching in the PubMed database identified clinical studies and basic research experiments in relation with the role of inflammation in BPH. Large clinical studies recently highlighted a relationship between chronic prostatic inflammation and prostate volume or urinary symptoms. Microscopic studies also found numerous inflammatory cells infiltrating BPH tissues. Immune cells are releasing cytokines and growth factors to modulate the immune response but evidences are also showing that they are promoting the epithelial and stromal prostatic cells growth. Moreover, prostatic cells by themselves are able to secrete inflammatory mediators and finally to stimulate their own growth. Once the vicious circle has started, it appears that feedback controls can be overwhelmed and that prostate volume progressively increases. BPH is a complex disease but chronic prostatic inflammation is one of the mechanisms leading to prostatic enlargement and urinary symptoms.