IL-17 is not essential for prostate inflammation and chronic pelvic pain development in an experimental model of chronic prostatitis/chronic pelvic pain syndrome

Autores
Motrich, Ruben Dario; Breser, Maria Laura; Sanchez, Leonardo Rodolfo; Godoy, Gloria Janet; Prinz, Immo; Rivero, Virginia Elena
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Pain and inflammation in the absence of infection are hallmarks in Chronic Prostatitis/Chronic Pelvic Pain Syndrome (CP/CPPS) patients. The etiology of CP/CPPS is unclear and autoimmunity has been proposed as a cause. Experimental Autoimmune Prostatitis (EAP) models have long been used for studying CP/CPPS. Herein, we studied prostate inflammation induction and chronic pelvic pain development in EAP using IL-12p40-KO, IL-4-KO, IL-17-KO, and wild type (C57BL/6) mice. Prostate antigen (PAg)-immunization in C57BL/6 mice induced specific Th1 and Th17 immune responses and severe prostate inflammation and cell infiltration, mainly composed of CD4+ T cells and macrophages. Moreover, chronic pelvic pain was evidenced by increased allodynia responses. In immunized IL-17-KO mice, the presence of a prominent PAg-specific Th1 immune response caused similar prostate inflammation and chronic pelvic pain. Furthermore, markedly high PAg-specific Th1 immune responses, exacerbated prostate inflammation, and chronic pelvic pain were detected in immunized IL-4-KO mice. Conversely, immunized IL-12p40-KO mice developed PAg-specific Th2 immune responses, characterized by high IL-4 secretion, and neither infiltration nor damage in the prostate. As observed in wild type control animals, IL12p40-KO mice did not evidence tactile allodynia responses. Our results suggest that, as in patients, chronic pelvic pain is a consequence of prostate inflammation. After PAg immunization, a Th1 associated immune response develops and induces prostate inflammation and chronic pelvic pain. The absence of Th1 or Th2 cytokines respectively diminishes or enhances EAP susceptibility. In addition, IL-17 showed not to be essential for pathology induction and chronic pelvic pain development.
Fil: Motrich, Ruben Dario. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Breser, Maria Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Sanchez, Leonardo Rodolfo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Godoy, Gloria Janet. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Prinz, Immo. Institute Of Immunology. Hannover Medical School; Alemania
Fil: Rivero, Virginia Elena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Materia
Pain
Inflammation
Chronic Prostatitis
Chronic Pelvic
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/46279
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/46279
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling IL-17 is not essential for prostate inflammation and chronic pelvic pain development in an experimental model of chronic prostatitis/chronic pelvic pain syndromeMotrich, Ruben DarioBreser, Maria LauraSanchez, Leonardo RodolfoGodoy, Gloria JanetPrinz, ImmoRivero, Virginia ElenaPainInflammationChronic ProstatitisChronic Pelvichttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Pain and inflammation in the absence of infection are hallmarks in Chronic Prostatitis/Chronic Pelvic Pain Syndrome (CP/CPPS) patients. The etiology of CP/CPPS is unclear and autoimmunity has been proposed as a cause. Experimental Autoimmune Prostatitis (EAP) models have long been used for studying CP/CPPS. Herein, we studied prostate inflammation induction and chronic pelvic pain development in EAP using IL-12p40-KO, IL-4-KO, IL-17-KO, and wild type (C57BL/6) mice. Prostate antigen (PAg)-immunization in C57BL/6 mice induced specific Th1 and Th17 immune responses and severe prostate inflammation and cell infiltration, mainly composed of CD4+ T cells and macrophages. Moreover, chronic pelvic pain was evidenced by increased allodynia responses. In immunized IL-17-KO mice, the presence of a prominent PAg-specific Th1 immune response caused similar prostate inflammation and chronic pelvic pain. Furthermore, markedly high PAg-specific Th1 immune responses, exacerbated prostate inflammation, and chronic pelvic pain were detected in immunized IL-4-KO mice. Conversely, immunized IL-12p40-KO mice developed PAg-specific Th2 immune responses, characterized by high IL-4 secretion, and neither infiltration nor damage in the prostate. As observed in wild type control animals, IL12p40-KO mice did not evidence tactile allodynia responses. Our results suggest that, as in patients, chronic pelvic pain is a consequence of prostate inflammation. After PAg immunization, a Th1 associated immune response develops and induces prostate inflammation and chronic pelvic pain. The absence of Th1 or Th2 cytokines respectively diminishes or enhances EAP susceptibility. In addition, IL-17 showed not to be essential for pathology induction and chronic pelvic pain development.Fil: Motrich, Ruben Dario. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Breser, Maria Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Sanchez, Leonardo Rodolfo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Godoy, Gloria Janet. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Prinz, Immo. Institute Of Immunology. Hannover Medical School; AlemaniaFil: Rivero, Virginia Elena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaElsevier Science2015-11info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/46279Motrich, Ruben Dario; Breser, Maria Laura; Sanchez, Leonardo Rodolfo; Godoy, Gloria Janet; Prinz, Immo; et al.; IL-17 is not essential for prostate inflammation and chronic pelvic pain development in an experimental model of chronic prostatitis/chronic pelvic pain syndrome; Elsevier Science; Pain; 157; 3; 11-2015; 585-5970304-39591872-6623CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://insights.ovid.com/crossref?an=00006396-201603000-00012info:eu-repo/semantics/altIdentifier/doi/10.1097/j.pain.0000000000000405info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:46:21Zoai:ri.conicet.gov.ar:11336/46279instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 09:46:21.344CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv IL-17 is not essential for prostate inflammation and chronic pelvic pain development in an experimental model of chronic prostatitis/chronic pelvic pain syndrome
title IL-17 is not essential for prostate inflammation and chronic pelvic pain development in an experimental model of chronic prostatitis/chronic pelvic pain syndrome
spellingShingle IL-17 is not essential for prostate inflammation and chronic pelvic pain development in an experimental model of chronic prostatitis/chronic pelvic pain syndrome
Motrich, Ruben Dario
Pain
Inflammation
Chronic Prostatitis
Chronic Pelvic
title_short IL-17 is not essential for prostate inflammation and chronic pelvic pain development in an experimental model of chronic prostatitis/chronic pelvic pain syndrome
title_full IL-17 is not essential for prostate inflammation and chronic pelvic pain development in an experimental model of chronic prostatitis/chronic pelvic pain syndrome
title_fullStr IL-17 is not essential for prostate inflammation and chronic pelvic pain development in an experimental model of chronic prostatitis/chronic pelvic pain syndrome
title_full_unstemmed IL-17 is not essential for prostate inflammation and chronic pelvic pain development in an experimental model of chronic prostatitis/chronic pelvic pain syndrome
title_sort IL-17 is not essential for prostate inflammation and chronic pelvic pain development in an experimental model of chronic prostatitis/chronic pelvic pain syndrome
dc.creator.none.fl_str_mv Motrich, Ruben Dario
Breser, Maria Laura
Sanchez, Leonardo Rodolfo
Godoy, Gloria Janet
Prinz, Immo
Rivero, Virginia Elena
author Motrich, Ruben Dario
author_facet Motrich, Ruben Dario
Breser, Maria Laura
Sanchez, Leonardo Rodolfo
Godoy, Gloria Janet
Prinz, Immo
Rivero, Virginia Elena
author_role author
author2 Breser, Maria Laura
Sanchez, Leonardo Rodolfo
Godoy, Gloria Janet
Prinz, Immo
Rivero, Virginia Elena
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv Pain
Inflammation
Chronic Prostatitis
Chronic Pelvic
topic Pain
Inflammation
Chronic Prostatitis
Chronic Pelvic
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Pain and inflammation in the absence of infection are hallmarks in Chronic Prostatitis/Chronic Pelvic Pain Syndrome (CP/CPPS) patients. The etiology of CP/CPPS is unclear and autoimmunity has been proposed as a cause. Experimental Autoimmune Prostatitis (EAP) models have long been used for studying CP/CPPS. Herein, we studied prostate inflammation induction and chronic pelvic pain development in EAP using IL-12p40-KO, IL-4-KO, IL-17-KO, and wild type (C57BL/6) mice. Prostate antigen (PAg)-immunization in C57BL/6 mice induced specific Th1 and Th17 immune responses and severe prostate inflammation and cell infiltration, mainly composed of CD4+ T cells and macrophages. Moreover, chronic pelvic pain was evidenced by increased allodynia responses. In immunized IL-17-KO mice, the presence of a prominent PAg-specific Th1 immune response caused similar prostate inflammation and chronic pelvic pain. Furthermore, markedly high PAg-specific Th1 immune responses, exacerbated prostate inflammation, and chronic pelvic pain were detected in immunized IL-4-KO mice. Conversely, immunized IL-12p40-KO mice developed PAg-specific Th2 immune responses, characterized by high IL-4 secretion, and neither infiltration nor damage in the prostate. As observed in wild type control animals, IL12p40-KO mice did not evidence tactile allodynia responses. Our results suggest that, as in patients, chronic pelvic pain is a consequence of prostate inflammation. After PAg immunization, a Th1 associated immune response develops and induces prostate inflammation and chronic pelvic pain. The absence of Th1 or Th2 cytokines respectively diminishes or enhances EAP susceptibility. In addition, IL-17 showed not to be essential for pathology induction and chronic pelvic pain development.
Fil: Motrich, Ruben Dario. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Breser, Maria Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Sanchez, Leonardo Rodolfo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Godoy, Gloria Janet. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Prinz, Immo. Institute Of Immunology. Hannover Medical School; Alemania
Fil: Rivero, Virginia Elena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
description Pain and inflammation in the absence of infection are hallmarks in Chronic Prostatitis/Chronic Pelvic Pain Syndrome (CP/CPPS) patients. The etiology of CP/CPPS is unclear and autoimmunity has been proposed as a cause. Experimental Autoimmune Prostatitis (EAP) models have long been used for studying CP/CPPS. Herein, we studied prostate inflammation induction and chronic pelvic pain development in EAP using IL-12p40-KO, IL-4-KO, IL-17-KO, and wild type (C57BL/6) mice. Prostate antigen (PAg)-immunization in C57BL/6 mice induced specific Th1 and Th17 immune responses and severe prostate inflammation and cell infiltration, mainly composed of CD4+ T cells and macrophages. Moreover, chronic pelvic pain was evidenced by increased allodynia responses. In immunized IL-17-KO mice, the presence of a prominent PAg-specific Th1 immune response caused similar prostate inflammation and chronic pelvic pain. Furthermore, markedly high PAg-specific Th1 immune responses, exacerbated prostate inflammation, and chronic pelvic pain were detected in immunized IL-4-KO mice. Conversely, immunized IL-12p40-KO mice developed PAg-specific Th2 immune responses, characterized by high IL-4 secretion, and neither infiltration nor damage in the prostate. As observed in wild type control animals, IL12p40-KO mice did not evidence tactile allodynia responses. Our results suggest that, as in patients, chronic pelvic pain is a consequence of prostate inflammation. After PAg immunization, a Th1 associated immune response develops and induces prostate inflammation and chronic pelvic pain. The absence of Th1 or Th2 cytokines respectively diminishes or enhances EAP susceptibility. In addition, IL-17 showed not to be essential for pathology induction and chronic pelvic pain development.
publishDate 2015
dc.date.none.fl_str_mv 2015-11
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/46279
Motrich, Ruben Dario; Breser, Maria Laura; Sanchez, Leonardo Rodolfo; Godoy, Gloria Janet; Prinz, Immo; et al.; IL-17 is not essential for prostate inflammation and chronic pelvic pain development in an experimental model of chronic prostatitis/chronic pelvic pain syndrome; Elsevier Science; Pain; 157; 3; 11-2015; 585-597
0304-3959
1872-6623
CONICET Digital
CONICET
url http://hdl.handle.net/11336/46279
identifier_str_mv Motrich, Ruben Dario; Breser, Maria Laura; Sanchez, Leonardo Rodolfo; Godoy, Gloria Janet; Prinz, Immo; et al.; IL-17 is not essential for prostate inflammation and chronic pelvic pain development in an experimental model of chronic prostatitis/chronic pelvic pain syndrome; Elsevier Science; Pain; 157; 3; 11-2015; 585-597
0304-3959
1872-6623
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://insights.ovid.com/crossref?an=00006396-201603000-00012
info:eu-repo/semantics/altIdentifier/doi/10.1097/j.pain.0000000000000405
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier Science
publisher.none.fl_str_mv Elsevier Science
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.069144

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