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Fluorescent acridine orange stain of difficult-to-grow coryneforms from expressed prostatic secretions. Magnification, ϫ 1,000.
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The laboratory diagnosis of acute bacterial prostatitis is straightforward and easily accomplished in clinical laboratories. Chronic bacterial prostatitis, and especially chronic idiopathic prostatitis (most often referred to as abacterial prostatitis), presents a real challenge to the clinician and clinical microbiologist. Clinically, the diagnosi...
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... observation and cul- ture of EPS on enriched media revealed the presence of these pleomorphic bacteria. Direct Gram staining of EPS showed gram-variable pleomorphic coccobacillary rods that did not grow on routine media within 72 h at 35°C. The presence of these pleomorphic swollen rods were also shown by fluorescent acridine orange staining (Fig. 1). Culture of the EPS demon- strated numerous rod-like forms on culture media enriched with yeast extract and horse serum and incubated for at least 72 h under 5% CO 2 at 35°C. EPS inoculated into tryptose broth demonstrated the presence of gram-variable rod forms (microscopically) and, when subcultured to routine and spe- cialized ...
Citations
... Intriguingly, prostate cancers are less likely the greater the frequency of ejaculations 77 (a proxy for the likelihood of vertical transmission). Although one might contend that the prostate gland is so well shielded from the environment that it would preclude any horizontal transmission from this organ, the prostate is a frequent target of infections (e.g., it is estimated that 70% of men suffer bacterial infections of their ll OPEN ACCESS 8 iScience 27, 110740, September 20, 2024 iScience Review prostate at some point in their lives 83 ). These infections are caused when bacteria get in the prostate when urine flows backward through the urethra (vesicoureteral reflux). ...
... These infections are caused when bacteria get in the prostate when urine flows backward through the urethra (vesicoureteral reflux). 83,84 Thus, this suggests that a selfish genetic element could be transmitted to and from the prostate through horizontal transmission via urine. ...
A growing number of studies have applied evolutionary and ecological principles to understanding cancer. However, few such studies have examined whether phenotypic plasticity––the ability of a single individual or genome to respond differently to different environmental circumstances––can impact the origin and spread of cancer. Here, we propose the adaptive horizontal transmission hypothesis to explain how flexible decision-making by selfish genetic elements can cause them to spread from the genome of their original host into the genomes of other hosts through the evolution of transmissible cancers. Specifically, we hypothesize that such cancers appear when the likelihood of successful vertical transmission is sufficiently low relative to the likelihood of successful horizontal transmission. We develop an evolutionary optimization model of this hypothesis, highlight empirical findings that support it, and offer suggestions for future research. Generally, phenotypically plastic selfish genetic elements might play an important role in the evolution of transmissible cancers.
... A number of pathogens are able to induce prostatitis, including viruses, fungi, bacteria and parasites (Nakai and Nonomura, 2013). The most commonly identified bacterium leading to prostatitis is the gram-negative bacterium E. coli (Domingue and Hellstrom, 1998). SActivation of TLRs on the cell surface and cytosolic nucleotide-binding and oligomerization domain (NOD) receptors, which play a major role in sensing bacterial components, also contribute to cancer progression (Kang et al., 2012;Moreira and Zamboni, 2012;Sfanos and De Marzo, 2012). ...
Chronic inflammation is known to contribute to various human cancers. Porphyromonas gingivalis (P. gingivalis), is a gram-negative oral keystone pathogen that may cause severe periodontitis and expresses several virulence factors to affect the host immune system. Periodontitis is a chronic infectious disease that while progression, may cause loss of attachment and destruction of the tooth supporting tissues. Prostate cancer is one of the most common malignancies in men. Increasing evidence links periodontitis with prostate cancer, however the mechanisms explaining this relationship remain unclear. The aim of this study was to investigate the expression and signaling pathway of programmed death ligand 1 (PD-L1) in a prostate cancer cell line after infection with P. gingivalis and stimulation with P. gingivalis components to reveal the mechanism of tumor-induced immune evasion associated with bacterial infection in the tumor environment. Prostate cancer cells were infected with different concentrations of viable P. gingivalis and treated with different concentrations of heat-killed P. gingivalis and P. gingivalis cell components, including the total membrane fraction, inner membrane fraction, outer membrane fraction, cytosolic fraction and peptidoglycan (PGN). Chemical inhibitors were used to block different important molecules of signaling pathways to assess the participating signal transduction mechanisms. PD-L1 expression was detected by Western blot after 24 h of infection. PD-L1 was demonstrated to be upregulated in prostate cancer cells after infection with viable and with heat-killed P. gingivalis membrane fractions. Also isolated PGN induced PD-L1 up-regulation. The upregulation was mediated by the NOD1/NOD2 signaling pathway. No upregulation could be detected after treatment of the cells with P. gingivalis lipopolysaccharide (LPS). These results indicate, that chronic inflammatory disease can contribute to tumor immune evasion by modifying the tumor microenvironment. Thus, chronic infection possibly plays an essential role in the immune response and may promote the development and progression of prostate cancer.
... The etiology and pathogenesis of nonbacterial prostatitis remains unclear. Causative factors that have been reported are Trichomonas vaginalis, Chlamydia trachomatis, genital mycoplasmas, staphylococci, coryneforms, genital viruses, biofilms, stagnation of prostatic secretion, autoimmune diseases, allergies, sex hormone disorders, and psychological factors.18-20 Even though several treatment strategies have been applied, it is still difficult to treat nonbacterial prostatitis. ...
The aim of this study was to investigate the anti-inflammatory effects of a new herbal formula (WSY-1075) in a nonbacterial prostatitis rat model.
Prostatitis was induced in male Wistar rats (n=32) by treatment with 17 beta-estradiol and dihydrotestosterone for 4 weeks. After the induction of prostatitis, the rats were randomly divided into one of four treatment groups: control (n=8), ciprofloxacin (n=8), WSY-1075 (100 mg/kg) (n=8), and WSY-1075 (400 mg/kg) (n=8). After 4 weeks of treatment, the prostatic proinflammatory cytokine (tumor necrosis factor-α, interleukin [IL]-6, and IL-8) levels and histological findings were noted.
The ciprofloxacin and WSY-1075 treatment groups showed significantly decreased proinflammatory cytokine levels compared with the control group. Histologically, treatment with ciprofloxacin and WSY-1075 significantly suppressed the severity of prostatitis lesions compared with those in the control group. No differences in the proinflammatory cytokine levels or histologic findings were observed with the dose dependent treatment of WSY-1075.
The new herbal formula, WSY-1075, showed effective anti-inflammatory activities in the prostate and may be useful for the clinical treatment of nonbacterial prostatitis. Our findings suggest that WSY-1075 has a beneficial effect on the prevention and treatment of nonbacterial prostatitis.
... Although it is well known that C. trachomatis causes urethritis, epididymitis, orchitis and chronic prostatitis, research focused on the pathogenic mechanisms involved in MGT infections is still very limited (Jantos et al., 1998;Domingue & Hellstrom, 1998;Pal et al., 2004;Skerk et al., 2004;Motrich et al., 2006;Wagenlehner et al., 2006;Cunningham & Beagley, 2008). Data from our laboratory demonstrated that rat prostate epithelial cells (PECs) were susceptible to infection with Chlamydia muridarum, a murine pathogen closely related to C. trachomatis (Mackern-Oberti et al., 2006). ...
Chlamydia trachomatis is an intracellular pathogen that infects mucosal epithelial cells, causing persistent infections. Although chronic inflammation is a hallmark of chlamydial disease, the proinflammatory mechanisms involved are poorly understood. Little is known about how innate immunity in the male genital tract (MGT) responds to C. trachomatis. Toll-like receptors (TLRs) are a family of receptors of the innate immunity that recognize different pathogen-associated molecular patterns (PAMPs) present in bacteria, viruses, yeasts and parasites. The study of TLR expression in the MGT has been poorly investigated. The aim of this work was to investigate the keratinocyte-derived chemokine (KC) response of MGT primary cultures from C57BL/6 mice to C. trachomatis and different PAMPs. KC production by prostate, seminal vesicle and epididymis/vas deferens cell cultures was determined by ELISA in culture supernatants. TLR2, 3, 4 and 9 agonists induced the production of KC by all MGT primary cultures assayed. In addition, we analysed the host response against C. trachomatis and Chlamydia muridarum. Chlamydial LPS (cLPS) as well as C. trachomatis and C. muridarum infection induced KC secretion by all MGT cell cultures analysed. Differences in KC levels were observed between cultures, suggesting specific sensitivity against pathogens among MGT tissues. Chemokine secretion was observed after stimulation of seminal vesicle cells with TLR agonists, cLPS and C. trachomatis. To our knowledge, this is the first report showing KC production by seminal vesicle cells after stimulation with TLR ligands, C. trachomatis or C. muridarum antigens. These results indicate that different receptors of the innate immunity are present in the MGT. Understanding specific immune responses, both innate and adaptive, against chlamydial infections, mounted in each tissue of the MGT, will be crucial to design new therapeutic approaches where innate and/or adaptive immunity would be targeted.
... Chronic wounds primarily afflict mildly immunocompromised individuals and thus the contaminating bacteria typically involve opportunistic pathogens, including the aquatic bacterium Pseudomonas aeruginosa [4]. Although not a common pathogen of individuals with a healthy immune system, P. aeruginosa has been demonstrated to be an opportunistic pathogen in ear infections [6], chronic bacterial prostatitis [7,8] and, most commonly, cystic fibrosis [9]. It is estimated that over one-half of all chronic wounds are colonised by P. aeruginosa [10]. ...
With an ageing and ever more obese population, chronic wounds such as diabetic ulcers, pressure ulcers and venous leg ulcers are an increasingly relevant medical concern. Identification of bacterial biofilm contamination as a major contributor to non-healing wounds demands biofilm-targeted strategies to manage chronic wounds. Pseudomonas aeruginosa has been identified as a principal biofilm-forming opportunistic pathogen in chronic wounds. The innate immune molecule lactoferrin and the rare sugar alcohol xylitol have been demonstrated to be co-operatively efficacious against P. aeruginosa biofilms in vitro. Data presented here propose a model for the molecular mechanism behind this co-operative antimicrobial effect. Lactoferrin iron chelation was identified as the primary means by which lactoferrin destabilises the bacterial membrane. By microarray analysis, 183 differentially expressed genes of ≥ 1.5-fold difference were detected. Interestingly, differentially expressed transcripts included the operon encoding components of the pyochelin biosynthesis pathway. Furthermore, siderophore detection verified that xylitol is the component of this novel synergistic treatment that inhibits the ability of the bacteria to produce siderophores under conditions of iron restriction. The findings presented here demonstrate that whilst lactoferrin treatment of P. aeruginosa biofilms results in destabilisation of the bacterial cell membrane though iron chelation, combined treatment with lactoferrin and xylitol inhibits the ability of P. aeruginosa biofilms to respond to environmental iron restriction.
... Since the etiology of nonbacterial prostatitis has not yet been established, various factors have been reported, including Trichomonas vaginalis, Chlamydia trachomatis, genital mycoplasmas, Staphylococci, Coryneforms, genital viruses, biofilm, stagnation of prostatic secretion, autoimmune diseases, allergy, sex hormone disorders, and psychological factors.21-23 In the present study, oxidative stress was investigated as a cause of CP. ...
Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS, NIH category III) accounts for 90-95% of prostatitis cases. However, standard treatment has not yet been established. It is known that polyphenols have an inhibitory effect on inflammation by their antioxidative capacity, and oligonol, a polyphenol derivative, has much higher bioavailability and bioactivity than common polyphenols. We investigated the anti-inflammatory effects and mechanisms of oligonol in estradiol-induced prostatitis rat models.
Prostatitis was induced by 17 beta-estradiol (E2) and dihydrotestosterone (DHT) in Wistar male rats (n = 20). Ten rats were placed in the oligonol-treated group and 10 in the E2 + DHT-treated group. The other 10 rats were also included as normal control group. Oligonol (60 mg/kg/day) was administered via gavage tube for 4 weeks. Superoxide dismutase (SOD), glutathione peroxidase (GPx), and tumor necrosis factor-alpha (TNF-alpha) were quantified, and phosphorylation of IkappaBa and histological changes were also evaluated in prostatic tissue.
The SOD and GPx activity showed tendencies to increase in the oligonol-treated group compared to the normal control group. TNF-alpha expression was slightly reduced in the oligonol-treated group. Western blotting demonstrated that phosphorylation of IkappaBa in the oligonol-treated group was significantly lower than in the normal control group. The E2 + DHT-treated group revealed severe atrophy of acinar epithelial cells and infiltration of leukocytes and lymphocytes in the prostate, however, the oligonol-treated group showed overall reduction in inflammatory features.
This study demonstrates that oligonol improves estradiol-induced non-bacterial prostatitis by regulating phosphorylation of IkappaBa. These findings suggest that oligonol has a beneficial effect on prevention and treatment of CP/CPPS.
... Bacterial infection of the prostate gland might have occurred from an ascending urethral infection or by reflux of infected urine into prostatic ducts emptying into the posterior urethra. Invasion of rectal bacteria by direct extension or by lymphogenous or haematogenous spread may also constitute other possible routes (Domingue & Hellstrom, 1998). Since the ESBL producer isolated from a purulent urethral discharge was not detected in other clinical samples including blood, urine, perinephric abscess and sputum, the prostatic abscess is the most probable source of this strain, while infected urine is the less likely source. ...
CTX-M-15 beta-lactamase-producing Klebsiella pneumoniae serotype K1 was isolated from a patient with fatal upper urinary tract infection (UTI) complicated by sepsis caused by K. pneumoniae serotype K2. Transfer of a CTX-M-15 beta-lactamase plasmid from the K1 to the K2 strain was observed. However, plasmid acquisition by the K2 strain did not occur in vivo, suggesting that the K1 strain might not have contributed directly to the upper UTI. In addition, effects of K serotypes and plasmid acquisition on K. pneumoniae serum resistance were examined.
... An underestimation of their representation due to a lack of specific investigation seems unlikely, considering the high rate of positive standard cultures in this age group; this rate is very similar to the rate observed in other age groups. These results are in accordance with recent studies reporting a low prevalence of venereal micro-organisms, and do not support the recommendations suggesting to treat first for Neisseiria gonorrhea and Chlamydiae trachomatis in young adults [28,26,30,4]. ...
There is currently a lack of consensus for the diagnosis, investigations and treatments of acute bacterial prostatitis (AP).
The symptoms, investigations and treatments of 371 inpatients diagnosed with AP were analyzed through a retrospective study conducted in four departments - Urology (U), Infectious Diseases (ID), Internal Medicine (IM), Geriatrics (G) - of two French university hospitals.
The cause of admission, symptoms, investigations and treatments depended markedly on the department of admission but not on the hospital. In U, patients commonly presented with a bladder outlet obstruction, they had a large imaging and functional check-up, and received alpha-blockers and anti-inflammatory drugs. In ID, patients were febrile and received longer and more appropriate antibiotic treatments. In G, patients presented with cognitive disorders and commonly had post-void urine volume measurements. In IM, patients presented with a wide range of symptoms, and had very diverse investigations and antibiotic regimen.Overall, a 3:1 ratio of community-acquired AP (CA-AP) to nosocomial AP (N-AP) was observed. Urine culture isolated mainly E. coli (58% of AP, 68% of CA-AP), with venereal agents constituting less than 1%. The probabilistic antibiotic treatments were similar for N-AP and CA-AP (58% bi-therapy; 63% fluoroquinolone-based regimen). For N-AP, these treatments were more likely to be inadequate (42% vs. 8%, p < 0.001) and had a higher rate of bacteriological failure (48% vs. 19%, p < 0.001). Clinical failure at follow-up was more common than bacteriological failure (75% versus 24%, p < 0.001). Patients older than 49 had more underlying urinary tract disorders and a higher rate of clinical failure (30% versus 10%, p < 0.0001).
This study highlights the difficulties encountered on a daily basis by the physicians regarding the diagnosis and management of acute prostatitis.
... A number of micro-organisms are able to infect the reproductive tract tissues in humans with serious consequences for reproductive function (Domingue & Hellstrom, 1998;Everaert et al., 2003). A common result of microbial infection of the reproductive tract is prostatitis, a condition that may lead to transient or permanent infertility (Schoor, 2002;Everaert et al., 2003). ...
... Bacterial infection of the prostate may occur as a result of ascending urethral infection or by reflux of infected urine into prostatic ducts emptying into the posterior urethra (Terai et al., 2000). Other possible routes of prostatitis include invasion of bacteria by lymphogenous or haematogenous spread (Domingue & Hellstrom, 1998). Chronic bacterial prostatitis (CBP) is a subtle illness, characterized by the persistence of bacteria in the prostatic secretory system (Schoor, 2002;Everaert et al., 2003). ...
... Chronic bacterial prostatitis (CBP) is a subtle illness, characterized by the persistence of bacteria in the prostatic secretory system (Schoor, 2002;Everaert et al., 2003). The most common causative agents of CBP are coagulase-negative staphylococci (CNS) and Staphylococcus aureus (Lowentritt et al., 1995;Domingue & Hellstrom, 1998;Ivanov, 2005). As it is difficult to establish precisely the significance of various micro-organisms in the pathogenesis of CBP, it is imperative to delineate both microbial and host factors that contribute to its development (Domingue & Hellstrom, 1998;Schoor, 2002;Hua et al., 2005). ...
This study reports the detection of an extracellular staphylococcal product, designated secretory inhibitor of platelet microbicidal protein (SIPMP), that causes local inhibition of the bactericidal action of platelet microbicidal protein (PMP) in the fluid phase. Urethral isolates of Staphylococcus aureus (n=24) and coagulase-negative staphylococci (CNS) (n=47) from patients with or without chronic bacterial prostatitis (CBP) were tested. SIPMP production was tested by inhibition of PMP bioactivity against Bacillus subtilis and was expressed as percentage inhibition of PMP bactericidal activity. The PMP susceptibility of staphylococcal strains was determined by exposing bacterial cells to serial dilutions of PMP. Staphylococci from patients without CBP produced SIPMP at levels of 10.3+/-1.2 and 13.25+/-1.72 % for S. aureus and CNS, respectively. Strains isolated from men with CBP inhibited PMP-induced killing of B. subtilis by 23.38+/-4.2 % (P<0.05) and 23.69+/-1.87 % (P<0.01) for S. aureus and CNS, respectively. SIPMP production correlated with staphylococcal resistance to PMP (r2=0.6082 and 0.7264 for S. aureus and CNS, respectively). SIPMP represents a hitherto unrecognized determinant of staphylococcal pathogenicity. These results suggest that SIPMP production is associated with the CBP source. Data from this study may have significant implications for the understanding of the pathogenesis of CBP.
Background
As one of the most common diseases in urology, a large number of preclinical studies have been accumulated to explore the etiological mechanism and potential intervention of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS).
Methods
In this study, we systematically evaluated the current status of preclinical research on CP/CPPS through bibliometrics analysis using VOSviewer and Citespace. Characteristics of publication such as year, country/region, institution, author, journal, citation, and keywords were analyzed. Based on the bibliometrics analysis results of keywords, we summarized the possible mechanisms and promising treatments for CP/CPPS narratively.
Results
According to the results of this study, the most common mechanisms involved in CP/CPPS were as follows: Disturbed immune and inflammation mediators, immune cell dysfunction, oxidative stress, dysregulated signaling pathways, apoptosis, gut microbiota, and testosterone metabolism. Traditional Chinese Medicine and extracorporeal shock wave therapy have important potential in the treatment of CP/CPPS.
Conclusion
Further translational studies targeting the above mechanisms and validating the objective efficacy of potential treatments indicated by preclinical studies in clinical patients are needed in the future.
