Urogenital Infections and Inflammations

T.E. Bjerklund Johansen, F. M.E. Wagenlehner, Y.-H. Cho, T. Matsumoto, J. N. Krieger, D. Shoskes, K. Naber

Etiology of chronic prostatitis/chronic pelvic pain syndrome – How animal models guide understanding of the syndrome

Stephen F. Murphy 1
 Praveen Thumbikat 2

1 Department of Urology, Feinberg School of Medicine, Northwestern University, Chicago, United States
2 Department of Urology, Chicago, United States


There remains a limited understanding of the etiology of CPPS. Given the diffuse nature of the symptoms and the heterogeneous nature of the patient population this is not surprising. Of the information that exists it is possible that further subdividing the patient population based on certain inflammatory criteria might be useful in basic research on CPPS going forward. Our laboratory and others have begun to understand and regard CPPS as an underlying autoimmune defect that is exacerbated by damage to the prostate resulting in a chronic symptomology. Much of this robust information on the emergence of CPPS has come from research performed in murine models of the disease.

Human studies

Various studies have sought to determine an association between CPPS and immune activation using samples from multiple sources including, expressed prostatic secretion (EPS), seminal plasma, semen and urine. These have shown not only an increase in the number of infiltrating cells (activated T and B cells, granulocytes and macrophages) [1], [2] but also increased levels of the IL2 receptor [3], [4] and specific inflammatory cytokines including IL1b, IL6, IL8, IgA and TNFa [5], [6], [7], [8]. As yet investigators have failed to determine a specific prostate antigen responsible for driving the autoimmunity in patients but research has been successful in isolating Th1 T-cells specific to prostate specific antigen (PSA) [9] in the peripheral blood of CPPS patients in the absence of carcinogenesis [10]. Auto-reactive CD4 T-cells have also been identified that respond to the seminal plasma of patients [11]. Further investigation to narrow down specific antigens have revealed IgA antibodies against Ny-Co-7 and MAD-PRO-34, both prostate specific, in CPPS patients [12], [13]. Taken together this data suggests that in humans there is some evidence of auto-reactivity against the prostate, which could mediate CPPS. This is supported histologically with one study showing an increase in the number of CD8+ T-cells in the prostate of patients compared to controls [13], [14]. Studies from our laboratory using a high-throughput multiplex array for over 40 cytokines and chemokines has shown an increased level of IL7 expression in CPPS patients compared to controls, and demonstrated that increased levels of IL7 was also positively correlated with increases in patient reported symptoms [15]. These findings were corroborated in the experimental autoimmune prostatitis (EAP) murine model where we identified prostate specific increases in IL7 expression [15]. IL7 is a driver of T-cell differentiation and function [16], [17], [18] and as such these findings also point to an underlying immune defect in CPPS patients.

Experimental autoimmune prostatitis

The experimental autoimmune prostatitis model (EAP) is a xenogenic mouse model of CPPS that is induced by a sub-cutaneous injection of a prostate homogenate or specific prostate proteins and an adjuvant [19], [20]. The model was first investigated in Wistar rats and has since been adapted into alternative forms in mice [21]. Early studies seemed to suggest that development of prostatitis was dependent on the prostate steroid binding protein (PSBP) which is was a candidate for a specific antigenic driver of pain as when used alone could induce CPPS-symptoms [22], [23], [24]. Additional studies determined that other antigens within the prostate homogenate are also important. Depending on the adjuvant used there are multiple different inflammatory and adaptive immune responses that are mounted that account for associated symptoms. Our model of EAP uses a whole rat prostate homogenate and the Titermax adjuvant, which we have demonstrated results in increased number of Th17 cells in B6 and NOD animals [15], [20]. Other models using CFA (complete freuds adjuvant) as an adjuvant, drive a more Th1-type (Il12p40 specifically) [25], [26] response without the similar increase or necessity for Th17 cells, but have also been successful in driving development of chronic symptoms in mice [25]. This use of different adjuvants to result in similar phenotypes is of particular interest and suggest that it maybe a defect in the ability of patients to control T-cell activation (Th1 or Th17 responses) by T-regulatory cells that is the underlying problem in patients rather than an excess of activation. This is further exemplified by the propensity for development of prostatitis in aged NOD mice compared to their B6 or Balb/c counterparts [27]. The NOD mouse is used in diabetes research where T-cell immune activation against pancreatic B-islet cells has been demonstrated [28], [29]. In the study of CPPS, NOD mice consistently develop pain responses that are significantly higher than their B6 counterparts in EAP models while also being uniquely susceptible to the development of chronic tactile allodynia in the CP1-induced model, see below [30]. NOD mice have been shown to have genetic polymorphisms in two genes that regulate T-cell function, IDD3 and CTLA4 [31], both of which have specific roles in maturation and functioning of T-regulatory cells [32]. This suggests that loss of T-regulatory cell function in these mice may account for the development of spontaneous prostatitis and prime the prostate immune microenvironment to development of chronic symptoms when activated.

Using the EAP model our laboratory demonstrated that two chemokines previously demonstrated to be associated with CPPS in humans, chemokine C-C motif ligands 2 and 3 (CCL2 and CCL3) were increased in prostate tissues during disease progression [33]. CCL2, also known as MCP1 (monocyte chemotactic protein 1) and CCL3, also known as MIP1a (macrophage inflammation protein 1 alpha) have been associated with development of multiple autoimmune disorders including rheumatoid arthritis [34], [35], [36], [37], [38]. In CPPS patients both chemokines were increased in EPS samples compared to controls but only MIP1a was positively correlated with increased symptoms severity [39]. From the mouse model we demonstrated that CCL3 was increased only at later time-points (day 20) following EAP induction [33]. This suggests that in patients as well as in mice that increased expression of certain chemokines may be dependent on when during disease course samples are collected and analyzed. Such differences may account for continuing difficulty in identifying a robust biomarker for CPPS as the immune microenvironment may be constantly shifting and changing.

Tryptase/PAR2/Mast cells

One cell type in particular that has emerged as a potential major mediator of inflammation and development of centralized pain in CPPS, the mast cell. Data from both human and mouse studies have revealed a central role for these cells in maintenance of chronic symptoms [21], [40], [41], [42], [43], [44], [45], [46], [47]. Mast cells are hematopoietic in nature and circulate in an immature form only differentiating fully once tissue resident. Such developmental processes are not unique to this cell type but do suggest some tissue specific cellular phenotype. These cells function as one of primary immune mediators to pathogenic infection and have multiple additional roles including tissue remodeling. Degranulation of mast cells upon activation is triggered by a variety of signals including the cytokine milieu, hormonal changes, physical changes and specific damage/pathogen-associated molecular patterns (D/PAMPs) [46]. Degranulation results in release of numerous factors and damage response elements, such as serotonin, prostaglandins, histamine and tryptase. In human disease mast cells are associated with a variety of autoimmune disorders including RA [40], [45], [48], [49], [50], [51], where increased numbers of cells and associated tryptase has been shown at affected sites. Mast cells have been shown to interact directly with T-cells both pro-inflammatory, Th17 cells and T-regulatory cells via the OX40 ligand [48], [52].

EPS from CPPS patients compared to controls has also been shown to have an increased level of tryptase and an increased number of mast cells [53]. Tryptase activates the protease-activated receptor 2 (PAR2), a member of the G-protein coupled receptor (GCPR) family that has known functions in pain and inflammation. The tryptase: PAR2 axis has been shown to be important for viseral pain and immune responses in ulcerative colitis and Crohn’s disease [54]. Our laboratory has demonstrated significant increases in the levels of tryptase and carboxypeptidase A (CPA3) another mast cell released factor in EPS samples from patients, indicating increased mast cell activity in CPPS [53]. Extending these findings into our murine EAP model we also demonstrated that PAR2 global knock-out mice are resistant to the development of pain upon EAP induction. Loss of PAR2 receptor expression appears to ablate MAPK/ERK signaling at the level of the dorsal root ganglion (DRG) associated with the prostate. We hypothesize that the mast cell might therefore mediate cross-talk between the immune response and the neurologic system in CPPS development [53]. Inhibition of PAR2 receptor activity therapeutically, using a blocking antibody, ameliorates tactile allodynia in mice and we are currently implementing the use of mast cell stabilizers clinically as part of a small trial. Taken together these data suggest that immunological activation may enhance mast cell activity, which can serve to coordinate neurological interactions resulting in chronic pain [53].

Bacteria in CPPS

While there is mounting evidence for the role of the immune system in the etiology of CPPS it is by no means well defined. Underpinning this is the source of the initial prostate damage. Our studies and others are beginning to determine that certain bacteria may be our best hope to further understanding this syndrome. Although CPPS is distinguished from the other sub-categories of prostatitis by the absence of an associated bacterial infection, bacteria can readily be detected and isolated from both EPS and urine samples. Comparisons of the microbiome isolated from voided bladder (VB) samples between patients and control samples have been performed and have not, as yet, demonstrated significant shifts in the microbial ecology [55], [56]. Currently as part of the MAPP project, research is underway that examines differences in the intestinal microbiome of patients versus controls. While these studies are useful from a therapeutic standpoint there is still a need to resolve deeper information into the etiology of the syndrome. A more robust approach from an etiological standpoint might be a deeper longitudinal characterization of microbiome shifts within the urogenital tract of patients to identify bacterial species that are prostate localized that are associated with CPPS symptoms over time. To this end our laboratory has focused on examining prostate localized bacterial isolates from CPPS patients to determine the role of specific human microbes in driving disease.

CP-1 (chronic-pain 1) is a prostate localized E. coli strain that was isolated from the EPS of a CPPS patient with active disease [30]. Our laboratory has demonstrated that intra-urethral infection with this bacterial species can induce chronic tactile allodynia in NOD but not B6 mice. Immune responses to the bacterial infection skew towards a Th17 response and infiltration of leukocytes to the prostate and inflammation are sustained after bacterial clearance [57]. We further demonstrate in this study that this immune activation and subsequent development of symptoms is transferable by adoptive transfer of ex vivo expanded T-cells that are skewed towards a Th17 phenotype [57]. It is important to note that to date no specific role for Th17 cells has been identified from human cells and the current data is mainly correlative. The specificity of these data was further demonstrated by comparison with a cystitis associated pathogenic E. coli strain, NU14, which failed to mount similar responses and did not result in development of chronic pain. These strains are evolutionarily distinct CP1 belonging to UPEC group B1 while NU14 is a group B2 strain. Further analysis revealed that NU14 is equally capable of adhering to prostate epithelial cells but that CP1 is inherently more invasive [58]. These studies underlined the bacterial specificity that we hypothesize to be very important in development and initiation of CPPS in humans. Furthermore this evidence also supports the theory that initial damage, such as a bacterial infection in certain genetic contexts can mount immune responses that fail to be controlled adequately resulting in development of chronic symptoms. The ability of the microbial ecology of the prostate to influence the immune microenvironment was examined further through our investigation on the potential of a commensal non-pathogenic bacterial strain, isolated from the prostate of a healthy man to control immune activation and ameliorate pain. Using our EAP model we demonstrate that intra-urethral instillation with a gram-positive Staphylococcus epidermidis species designated NPI (non-pain inducing), could reverse EAP-associated IL17 expression and significantly reduce tactile allodynia responses [59]. NPI alone does not induce tactile allodynia in either B6 or NOD mice but is capable of colonizing prostate tissues in both animal backgrounds. More recently we are examining the effect of instillation of this bacteria in the context of an ongoing CP1 infection and are demonstrating that NPI colonization can prevent CP1-induced pain from developing. Taken together these findings demonstrate that specific bacteria from the prostate may have a role in initiation of CPPS in humans, that this can be maintained in the absence of an ongoing infection and most importantly that it can be reversed upon restoration of healthy immune: microbial interactions.

To further emphasize this point we are currently examining the potential of gram-positive bacterial species, isolated from the EPS of CPPS patients to induce pain in mice. In prostatitis diagnoses, including CPPS, gram-positive bacteria are usually deemed clinically insignificant and traditional uropathogens are thought to be gram-negative in nature. We have observed however that gram-positive species make up a large proportion of the bacterial content of the EPS and that when isolated from patient samples are capable of potentiating disease in a manner similar to CP1. Our initial studies suggest that intra-urethral instillation with three of these strains, S. epidermidis, E. faecalis, and S. hemolyticus, induces chronic tactile allodynia in NOD but not B6 animals. Furthermore characterization of the immune response of these animals to bacterial infection reveals that it is not mediated by Th17 cells but may involved NK-cell immune activation. These findings further support our hypothesis that it is loss of regulatory control of immune responses in these mice that result in CPPS-like symptom emergence rather than a particular flavor of adaptive immune response. This mirrors the seemingly conflicting evidence from the different EAP murine models of CPPS, which have shown opposing inflammatory processes to be dispensable and/or necessary for inflammation and pain development.


We have presented here the current understanding of the etiology of CPPS from a microbial and immunological perspective. From studies using both patient samples and murine models we postulate that it is the inter-play between bacteria and the immune system that is the major initiator of the syndrome and symptoms are then maintained owing to a host genetic defect in regulation of the adaptive immune response. Large patient-focused studies on the ongoing immune response throughout symptom maintenance and also the urinary microbiome changes in patients are necessary to further delineate this and more importantly to uncover potential therapeutics.


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[57] Quick ML, Wong L, Mukherjee S, Done JD, Schaeffer AJ, Thumbikat P. Th1-Th17 cells contribute to the development of uropathogenic Escherichia coli-induced chronic pelvic pain. PLoS ONE. 2013;8(4):e60987. DOI: 10.1371/journal.pone.0060987
[58] Rudick CN, Billips BK, Pavlov VI, Yaggie RE, Schaeffer AJ, Klumpp DJ. Host-pathogen interactions mediating pain of urinary tract infection. J Infect Dis. 2010 Apr;201(8):1240-9. DOI: 10.1086/651275
[59] Murphy SF, Schaeffer AJ, Done JD, Quick ML, Acar U, Thumbikat P. Commensal bacterial modulation of the host immune response to ameliorate pain in a murine model of chronic prostatitis. Pain. 2017 Aug;158(8):1517-1527. DOI: 10.1097/j.pain.0000000000000944

The ZB MED – Information Center for Life Sciences, Germany, together with the European Association of Urology (EAU) provided the opportunity to publish a “Living Textbook” on “Urogenital Infections and Inflammations” in an open access form. This “Living Textbook” represents also an update of the Textbook on Urogenital Infections published 2010 by the International Consultation on Urological Infections and the EAU: http://www.icud.info/urogenitalinfections.html.

The “Living Textbook” will cover infections and inflammations of the kidney, the urinary tract, as well as the male and female genital tract considering pathogenesis, diagnostics, treatment, prophylaxis and future aspects. The “Living Textbook” will be structured into about 26 Sections each with two section co-chairs responsible for peer review of the chapters of each section. Each chapter should reflect the background to the topic and highlight all of the critical evidence relating to the subject. The intention is to provide an up to date, concise synthesis of the literature on that topic, and for clinical topics also recommendations based on levels of evidence for contemporary clinical practice, as well as suggested research recommendations.

The editors hope that this “Living Textbook” may become a useful instrument for physicians of different specialties taking care about patients suffering from these diseases.

Truls E. Bjerklund Johansen (Norway),

Florian ME Wagenlehner (Germany),

Yong-Hyun Cho (South Korea),

Tetsuro Matsumoto (Japan),

John N Krieger (USA),

Daniel Shoskes (USA),

Kurt G. Naber (Germany).

Publishing at PUBLISSO

Your chapter will be published at the PUBLISSO platform (https://books.publisso.de).

Information for corresponding authors

It is necessary for all corresponding authors to register at PUBLISSO.
To register at PUBLISSO please click the following link: http://books.publisso.de/publisso_gold/register

After registration, please complete your user profile. Information from your user profile will appear in the published chapter and the authors board of the book (http://books.publisso.de/publisso_gold/book/52). If you are displayed in the authors board, you can be contacted by readers and other professionals. You can also contact other authors of the book for exchange and to build a network.
(If you do not want to be displayed in the authors board, but stay registered, you can disable this feature in your profile settings. In this case, your affiliation (publication data) will be displayed in the published chapter only.)

We kindly ask you to provide the co-authors email addresses in the manuscript so that we can contact them in case of queries.

Information for co-authors

After publication of your chapter, your affiliation (publication data) will be displayed in the published chapter.

If you also want to be displayed in the authors board of the book (http://books.publisso.de/publisso_gold/book/52), we kindly ask you to register at PUBLISSO. If you are displayed in the authors board, you can be contacted by readers and other professionals. You can also contact other authors of the book for exchange and to build a network.

To register at PUBLISSO please click the following link: http://books.publisso.de/publisso_gold/register

If you do not want to be displayed in the authors board of the book, you do not have to register. Your affiliation (publication data) will be displayed in the published chapter only.


If you have any further questions please don’t hesitate to contact the PUBLISSO editorial office:

E-Mail: livingbooks@zbmed.de
Phone: +49 221 478-7093


The textbook will be structured in sections with two co-chairs each. Each section will start with an introductory chapter written by the two respective co-chairs presented like an editorial commentary in regard to the following chapters (see proposed contents of the book). The two co-chairs of each section will also peer review all chapters in their section and stimulate a consensus discussion within their section together with the authors and the main editors if needed.


Each chapter should reflect the background to the topic and highlight all of the critical evidence relating to the subject. The intention is to provide an up to date, concise synthesis of the literature on that topic, and for clinical topics also recommendations based on levels of evidence for contemporary clinical practice, as well as suggested research recommendations.


Each manuscript should have up to approximately 3,000 words (excluding abstract, tables/figures and references). The abstract should count about 300 words.


The outline of each chapter should be structured as follows (similar as in the edition 2010, which can be downloaded for free: http://www.icud.info/urogenitalinfections.html):

  1. Abstract
  2. Summary of recommendations*/key notes*
    (*which ever term is more appropriate)
  3. Introduction
  4. Methods
  5. Results
  6. Further research
  7. Conclusions
  8. Acknowledgement
  9. Conflict of interest of each author
  10. References

Citation style

As a citation style, the Vancouver style is preferred.

Please mark your references in the text with square brackets ([1], [2], ...).

Summary of recommendations

We would like to have the Summary of recommendations at the beginning after the abstract (as in the edition 2010). However, we do not expect as in the edition 2010, that each recommendation is also specified according to Level of Evidence and Grade of Recommendation, because such a claim would not only need a systematic literature search (see below), but also a structured discussion in a defined group of experts.

Systematic literature search

A systematic literature search should be performed, at least of PUBMED/MEDLINE but ideally of several relevant databases in addition (like Cochrane CENTRAL) to find recent, high quality systematic reviews and/or primary research studies. It is not expected to perform for all chapters a de novo systematic review, if such reviews are already published recently, but it still may be indicated for some items. For questions relating therapy, it should be focused on evidence from (systematic reviews of) randomized controlled trials if available.

The method of the systematic literature search needs to be fully described in the section “Methods”, e.g.:

“A systematic literature search was performed for the last ... (usually 10) years in MEDLINE, Cochrane etc. with the following key words ... and the following limitations: e.g. UTI, age (adult?), ... clinical studies ... English ... abstract available ... only peer reviewed ...

A total of ... publications were identified, which were screened by title and abstract ... After exclusion of duplicates ... a total of ... were included into the review (analysis), supplemented by citations or known to the authors ... ”.

Clinical topics

Clinical topics should be focused on the importance to clinical practice according to the up to date scientific knowledge as presented in the literature. It should relate to questions/complaints/symptoms of patient/population concerning definition, diagnosis, therapy/prevention, intervention, and outcome in comparison, if different approaches are feasible. Please choose patient-important outcomes and focus on those, which you deem critical for decision-making.

Level of evidence and grade of recommendations

Any recommendation should be based on the level of evidence and the grade of recommendation. For this purpose the following system, modified from the Oxford Centre for Evidence-based Medicine should be used (EAU guidelines 2015):

Level of evidence (LE)

Level Type of evidence
1a Evidence obtained from meta-analysis of randomised trials
1b Evidence obtained from at least one randomised trial
2a Evidence obtained from one well-designed controlled study without randomization
2b Evidence obtained from at least one other type of well-designed quasi-experimental study
3 Evidence obtained from well-designed non-experimental studies, such as comparative studies, correlation studies and case reports.
4 Evidence obtained from expert committee reports or opinions or clinical experience of respected authorities.

Grade of Recommendations (GoR)

Grade Nature of recommendations
A Based on clinical studies of good quality and consistency addressing the specific recommendations and including at least one randomised trial
B Based on well-conducted clinical studies, but without randomised clinical trials
C Made despite the absence of directly applicable clinical studies of good quality

Comments (EAU guidelines 2015)

The aim of assigning a LE and grading recommendations is to provide transparency between the underlying evidence and the recommendation given.

It should be noted that when recommendations are graded, the link between the level of evidence and grade of recommendation is not directly linear. Availability of randomized controlled trials may not necessarily translate into a grade “A” recommendation where there are methodological limitations or disparity in published results.

Alternatively, absence of high level evidence does not necessarily preclude a grade A recommendation, if there is overwhelming clinical experience and consensus. In addition, there may be exceptional situations where corroborating studies cannot be performed, perhaps for ethical or other reasons and in this case unequivocal recommendations are considered helpful for the reader. The quality of the underlying scientific evidence - although a very important factor – has to be balanced against benefits and burdens, values and preferences and costs when a grade is assigned.

Since the same rating system should be used in all chapters, for the sake of brevity the same sentence could be used in “Methods” for all manuscripts, because the rating system will be described in details in the Preface of the book:

“The studies were rated according to the level of evidence and the strength of recommendations graded according to a system used in the EAU guidelines modified from the Oxford Centre for Evidence-based Medicine [1].”


[1] European Association of Urology. Guidelines. Methodology section. 2015 ed. Arnhem: European Association of Urology; 2015. p. 3. ISBN/EAN: 978-90-79754-80-9. Available from: http://uroweb.org/wp-content/uploads/EAU-Extended-Guidelines-2015-Edn..pdf

The Living Handbook of Urogenital Infections and Inflammations is issued by:

European Association of Urology
att. Maurice Schlief, EAU executive manager business affairs

P.O.Box 30016
NL-6803 AA Arnhem, The Netherlands

Phone: 0031-26-38.90.680
E-mail: m.schlief@uroweb.org

Editor in Chief

responsible for the contents according to § 5 TMG and § 55 Abs. 2 RStV (Germany):

Kurt G. Naber, MD, PhD
Assoc. Professor of Urology

Technical University of Munich
Karl-Bickleder-Str. 44c
94315 Straubing, Germany

E-mail: kurt.naber@nabers.de

John N. Krieger MD, PhD

University of Washington Section of Urology


Daniel Shoskes MD, PhD

Cleveland Clinic Glickman Urological and Kidney Institute


Yong-Hyun Cho MD, PhD

St. Mary's Hospital, The Catholic University of Korea Department of Urology


Tetsuro Matsumoto MD, PhD

University of Occupational and Environmental Health Department of Urology


Florian M. E. Wagenlehner MD, PhD

Justus-Liebig University of Giessen Clinic of Urology and Andrology


Truls Erik Bjerklund Johansen MD, PhD

Oslo University Hospital Urology Department


Kurt G. Naber MD, PhD

Technical University of Munich


Punit Bansal MD, PhD

R G Stone and Super Specialty Hospital
Department of Urology


Riccardo Bartoletti

University of Pisa
Department of Translational Research and New Technologies


Truls Erik Bjerklund Johansen MD, PhD

Oslo University Hospital
Urology Department


PD Dr. med. Gernot Bonkat

University Basel
alta uro AG, Merian Iselin Klinik, Center of Biomechanics & Calorimetry (COB)


Prof. Tommaso Cai MD

Santa Chiara Regional Hospital
Dept. of Urology


Dr Leyland Chuang

Ng Teng Fong Hospital, National University Health System
Department of Medicine


Prof. Milan Cizman

University Medical Centre
Department of Infectious Diseases


Alison Crawford MSc

Queen's University
Department of Psychology


Pfofessor Svetlana Dubrovina MD, PhD

Rostov Medical State University
Obstetrics and Gynaecology


Dr Valerie Huei Li Gan MBBS (S'pore), MRCS (Edin), MMed (Surg), FAMS (Urology)

Singapore General Hospital
Department of Urology


Philip Hanno

University of Pennsylvania


Ass prof MD Gundela Holmdahl

Queen Silvia Childrens Hospital, Sahlgrens Academy
Pediatric surgery and urology


Udo B. Hoyme

HELIOS Hospital Erfurt Ltd.
Department of Gynecology and Obstetrics


David Hunstad

Washington University School of Medicine
Pediatrics / Molecular Microbiology


Gitte M. Hvistendahl

Aarhus University Hospital


Prof. Michael KOGAN M.D., PhD

Rostov State Medical University
Department of Urology


Dr Akihiro Kanematsu

Hyogo College of Medicine
Department of Urology


Frieder Keller

University Hospital Ulm
Department Internal Medicine 1, Nephrology


Professor Katarzyna Kilis-Pstrusinska PhD, MD

Wroclaw Medical University
Department of Pediatric Nephrology


MD, PhD Tae-Hyoung Kim

Chung-Ang University


John N. Krieger MD, PhD

University of Washington
Section of Urology


Prof Ekaterina Kulchavenya

Novosibirsk Research TB Institute, Novosibirsk State Medical University


Dr Christina Kåbjörn Gustafsson

Ryhov Hospital Jönköping


Dr. Bela Köves

South Pest Teaching Hospital
Department of Urology


Dr. med. Giuseppe Magistro

Ludwig-Maximilians-University of Munich
Department of Urology


Vittorio Magri

Urologic Clinic


András Magyar

South-Pest Hospital
Department of Urology


Professor Emeritus Brian Morris

University of Sydney
School of Medical Sciences


Baerbel Muendner-Hensen

ICA-Deutschland e.V.


Stephen F. Murphy

Feinberg School of Medicine, Northwestern University
Department of Urology


Kurt G. Naber MD, PhD

Technical University of Munich


Prof. Yulia Naboka

Rostov State Medical University
Department of Microbiology


Dr. J. Curtis Nickel MD

Queen's University
Department of Urology


Professor Ralph Peeker MD PhD

University of Gothenburg
Department of Urology


Tamara Perepanova

N.A. Lopatkin Research Institute of Urology and Interventional Radiology


Prof. Gianpaolo Perletti M. Clin. Pharmacol.

University of Insubria
Department of Biotechnology and Life Sciences


Felice Petraglia

Department of Biomedical, Experimental and Clinical Sciences, University of Florence
Obstetrics and Gynecology


Michel Pontari

Temple University School of Medicine
Department of Urology


Dr. Jörgen Quaghebeur PhD. Med. Sci.

University Hospital Antwerp and University Antwerp
Department of Urology


Yazan F. Rawashdeh

Aarhus University Hospital
Paediatric Urology Section, Department of Urology


Professor Claus Riedl MD



Matthew Roberts

The University of Queensland
Faculty of Medicine


PD Dr. med Guido Schmiemann MPH

Institut für Public Health und Pflegeforschung, Universität Bremen
Abteilung Versorgungsforschung


Caroline Schneeberger MD PhD

Academic Medical Center (AMC)


Prof. Dr. med. Peter Schneede

Klinikum Memmingen
Department of Urology


Aaron C. Shoskes

Des Moines University Medical College of Ostheopathic Medicine


Daniel Shoskes MD, PhD

Cleveland Clinic
Glickman Urological and Kidney Institute


Prof. Dr. Roswitha Siener

University of Bonn
University Stone Centre, Department of Urology


Sofia Sjöström

Queen Silvia Childrens Hospital, Sahlgrens Academy
Pediatric surgery and urology


Mathew Sorensen

University of Washington School of Medicine
Department of Urology


Prof. Dr. Dr. Walter Ludwig Strohmaier FEBU

Regiomed-Klinikum Coburg. Medical School Regiomed
Urology and Paediatric Urology


Satoshi Takahashi

Sapporo Medical University School of Medicine
Department of Infection Control and Laboratory Medicine


Professor Paul Anantharajah Tambyah

Yong Loo Lin School of Medicine, National University Hospital
Department of Medicine


Peter Tenke

Jahn Ferenc South Pest Teaching Hospital
Department of Urology


Praveen Thumbikat

Department of Urology


Dr. Jose Tiran Saucedo

IMIGO / Universidad de Monterrey
Obstetrics and Gynaecology


Dominic Tran-Nguyen

Des Moines University


Dean Tripp

Queen's University
Psychology, Anesthesia & Urology



The Catholic University of Korea, St. Vincent's Hospital
Division of Infectious Diseases, Department of Internal Medicine


Florian M. E. Wagenlehner MD, PhD

Justus-Liebig University of Giessen
Clinic of Urology and Andrology


Assoc. Prof. Christian Wejse

Aarhus University, Aarhus University Hospital
Department of Infectious Diseases/Center for Global Health, Dept of Public Health


Prof. Dr. Mete Çek

Trakya University, School of Medicine