Depletion of dendritic cells enhances innate anti-bacterial host defense through modulation of phagocyte homeostasis

Autores
Autenrieth, Stella E.; Warnke, Philipp; Wabnitz, Guido H.; Lucero Estrada, Cecilia Stella Marys; Pasquevich, Karina Alejandra; Drechsler, Doreen; Gunter, Manina; Hochweller, Kristin; Novakovic, Ana; Beer Hammer, Sandra; Samstag, Yvonne; Hämmerling, Günter J.; Garbi, Natalio; Autenrieth, Ingo B.
Año de publicación
2012
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Dendritic cells (DCs) as professional antigen-presenting cells play an important role in the initiation and modulation of the adaptive immune response. However, their role in the innate immune response against bacterial infections is not completely defined. Here we have analyzed the role of DCs and their impact on the innate anti-bacterial host defense in an experimental infection model of Yersinia enterocolitica (Ye). We used CD11c-diphtheria toxin (DT) mice to deplete DCs prior to severe infection with Ye. DC depletion significantly increased animal survival after Ye infection. The bacterial load in the spleen of DC-depleted mice was significantly lower than that of control mice throughout the infection. DC depletion was accompanied by an increase in the serum levels of CXCL1, G-CSF, IL-1α, and CCL2 and an increase in the numbers of splenic phagocytes. Functionally, splenocytes from DC-depleted mice exhibited an increased bacterial killing capacity compared to splenocytes from control mice. Cellular studies further showed that this was due to an increased production of reactive oxygen species (ROS) by neutrophils. Adoptive transfer of neutrophils from DC-depleted mice into control mice prior to Ye infection reduced the bacterial load to the level of Ye-infected DC-depleted mice, suggesting that the increased number of phagocytes with additional ROS production account for the decreased bacterial load. Furthermore, after incubation with serum from DC-depleted mice splenocytes from control mice increased their bacterial killing capacity, most likely due to enhanced ROS production by neutrophils, indicating that serum factors from DC-depleted mice account for this effect. In summary, we could show that DC depletion triggers phagocyte accumulation in the spleen and enhances their anti-bacterial killing capacity upon bacterial infection.
Fil: Autenrieth, Stella E.. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; Alemania
Fil: Warnke, Philipp. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; Alemania
Fil: Wabnitz, Guido H.. Universität Heidelberg. Institut für Immunologie; Alemania
Fil: Lucero Estrada, Cecilia Stella Marys. Universidad Nacional de San Luis. Facultad de Quimica, Bioquimica y Farmacia. Area Microbiologia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; Alemania
Fil: Pasquevich, Karina Alejandra. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; Alemania
Fil: Drechsler, Doreen. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; Alemania
Fil: Gunter, Manina. Universität Tübingen. Interfakultäres Institut Für Zellbiologie; Alemania
Fil: Hochweller, Kristin. Deutsches Krebsforschungszentrum. Abteilung Molekulare Immunologie; Alemania
Fil: Novakovic, Ana. Institut Für Pharmakologie Und ToxikologieAbteilung für Pharmakologie und experimentelle Therapie, Institut für experimentelle und klinische Pharmakologie und Toxikologie, Universität Tübingen; Alemania
Fil: Beer Hammer, Sandra. Universität Tübingen; Alemania
Fil: Samstag, Yvonne. Universität Heidelberg; Alemania
Fil: Hämmerling, Günter J.. Deutsches Krebsforschungszentrum. Abteilung Molekulare Immunologie; Alemania
Fil: Garbi, Natalio. Deutsches Krebsforschungszentrum. Abteilung Molekulare Immunologie; Alemania. Universität Bonn; Alemania
Fil: Autenrieth, Ingo B.. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; Alemania
Materia
DENDRITIC CELLS
PHAGOCITES
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:11336/14618
Acceder
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network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Depletion of dendritic cells enhances innate anti-bacterial host defense through modulation of phagocyte homeostasisAutenrieth, Stella E.Warnke, PhilippWabnitz, Guido H.Lucero Estrada, Cecilia Stella MarysPasquevich, Karina AlejandraDrechsler, DoreenGunter, ManinaHochweller, KristinNovakovic, AnaBeer Hammer, SandraSamstag, YvonneHämmerling, Günter J.Garbi, NatalioAutenrieth, Ingo B.DENDRITIC CELLSPHAGOCITEShttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Dendritic cells (DCs) as professional antigen-presenting cells play an important role in the initiation and modulation of the adaptive immune response. However, their role in the innate immune response against bacterial infections is not completely defined. Here we have analyzed the role of DCs and their impact on the innate anti-bacterial host defense in an experimental infection model of Yersinia enterocolitica (Ye). We used CD11c-diphtheria toxin (DT) mice to deplete DCs prior to severe infection with Ye. DC depletion significantly increased animal survival after Ye infection. The bacterial load in the spleen of DC-depleted mice was significantly lower than that of control mice throughout the infection. DC depletion was accompanied by an increase in the serum levels of CXCL1, G-CSF, IL-1α, and CCL2 and an increase in the numbers of splenic phagocytes. Functionally, splenocytes from DC-depleted mice exhibited an increased bacterial killing capacity compared to splenocytes from control mice. Cellular studies further showed that this was due to an increased production of reactive oxygen species (ROS) by neutrophils. Adoptive transfer of neutrophils from DC-depleted mice into control mice prior to Ye infection reduced the bacterial load to the level of Ye-infected DC-depleted mice, suggesting that the increased number of phagocytes with additional ROS production account for the decreased bacterial load. Furthermore, after incubation with serum from DC-depleted mice splenocytes from control mice increased their bacterial killing capacity, most likely due to enhanced ROS production by neutrophils, indicating that serum factors from DC-depleted mice account for this effect. In summary, we could show that DC depletion triggers phagocyte accumulation in the spleen and enhances their anti-bacterial killing capacity upon bacterial infection.Fil: Autenrieth, Stella E.. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; AlemaniaFil: Warnke, Philipp. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; AlemaniaFil: Wabnitz, Guido H.. Universität Heidelberg. Institut für Immunologie; AlemaniaFil: Lucero Estrada, Cecilia Stella Marys. Universidad Nacional de San Luis. Facultad de Quimica, Bioquimica y Farmacia. Area Microbiologia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; AlemaniaFil: Pasquevich, Karina Alejandra. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; AlemaniaFil: Drechsler, Doreen. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; AlemaniaFil: Gunter, Manina. Universität Tübingen. Interfakultäres Institut Für Zellbiologie; AlemaniaFil: Hochweller, Kristin. Deutsches Krebsforschungszentrum. Abteilung Molekulare Immunologie; AlemaniaFil: Novakovic, Ana. Institut Für Pharmakologie Und ToxikologieAbteilung für Pharmakologie und experimentelle Therapie, Institut für experimentelle und klinische Pharmakologie und Toxikologie, Universität Tübingen; AlemaniaFil: Beer Hammer, Sandra. Universität Tübingen; AlemaniaFil: Samstag, Yvonne. Universität Heidelberg; AlemaniaFil: Hämmerling, Günter J.. Deutsches Krebsforschungszentrum. Abteilung Molekulare Immunologie; AlemaniaFil: Garbi, Natalio. Deutsches Krebsforschungszentrum. Abteilung Molekulare Immunologie; Alemania. Universität Bonn; AlemaniaFil: Autenrieth, Ingo B.. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; AlemaniaPublic Library of Science2012-02info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/14618Autenrieth, Stella E.; Warnke, Philipp; Wabnitz, Guido H.; Lucero Estrada, Cecilia Stella Marys; Pasquevich, Karina Alejandra; et al.; Depletion of dendritic cells enhances innate anti-bacterial host defense through modulation of phagocyte homeostasis; Public Library of Science; Plos Pathogens; 8; 2; 2-2012; 1-161553-7366enginfo:eu-repo/semantics/altIdentifier/url/http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1002552info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.ppat.1002552info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T11:16:50Zoai:ri.conicet.gov.ar:11336/14618instacron: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:34982025-10-22 11:16:50.612CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Depletion of dendritic cells enhances innate anti-bacterial host defense through modulation of phagocyte homeostasis
title Depletion of dendritic cells enhances innate anti-bacterial host defense through modulation of phagocyte homeostasis
spellingShingle Depletion of dendritic cells enhances innate anti-bacterial host defense through modulation of phagocyte homeostasis
Autenrieth, Stella E.
DENDRITIC CELLS
PHAGOCITES
title_short Depletion of dendritic cells enhances innate anti-bacterial host defense through modulation of phagocyte homeostasis
title_full Depletion of dendritic cells enhances innate anti-bacterial host defense through modulation of phagocyte homeostasis
title_fullStr Depletion of dendritic cells enhances innate anti-bacterial host defense through modulation of phagocyte homeostasis
title_full_unstemmed Depletion of dendritic cells enhances innate anti-bacterial host defense through modulation of phagocyte homeostasis
title_sort Depletion of dendritic cells enhances innate anti-bacterial host defense through modulation of phagocyte homeostasis
dc.creator.none.fl_str_mv Autenrieth, Stella E.
Warnke, Philipp
Wabnitz, Guido H.
Lucero Estrada, Cecilia Stella Marys
Pasquevich, Karina Alejandra
Drechsler, Doreen
Gunter, Manina
Hochweller, Kristin
Novakovic, Ana
Beer Hammer, Sandra
Samstag, Yvonne
Hämmerling, Günter J.
Garbi, Natalio
Autenrieth, Ingo B.
author Autenrieth, Stella E.
author_facet Autenrieth, Stella E.
Warnke, Philipp
Wabnitz, Guido H.
Lucero Estrada, Cecilia Stella Marys
Pasquevich, Karina Alejandra
Drechsler, Doreen
Gunter, Manina
Hochweller, Kristin
Novakovic, Ana
Beer Hammer, Sandra
Samstag, Yvonne
Hämmerling, Günter J.
Garbi, Natalio
Autenrieth, Ingo B.
author_role author
author2 Warnke, Philipp
Wabnitz, Guido H.
Lucero Estrada, Cecilia Stella Marys
Pasquevich, Karina Alejandra
Drechsler, Doreen
Gunter, Manina
Hochweller, Kristin
Novakovic, Ana
Beer Hammer, Sandra
Samstag, Yvonne
Hämmerling, Günter J.
Garbi, Natalio
Autenrieth, Ingo B.
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv DENDRITIC CELLS
PHAGOCITES
topic DENDRITIC CELLS
PHAGOCITES
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Dendritic cells (DCs) as professional antigen-presenting cells play an important role in the initiation and modulation of the adaptive immune response. However, their role in the innate immune response against bacterial infections is not completely defined. Here we have analyzed the role of DCs and their impact on the innate anti-bacterial host defense in an experimental infection model of Yersinia enterocolitica (Ye). We used CD11c-diphtheria toxin (DT) mice to deplete DCs prior to severe infection with Ye. DC depletion significantly increased animal survival after Ye infection. The bacterial load in the spleen of DC-depleted mice was significantly lower than that of control mice throughout the infection. DC depletion was accompanied by an increase in the serum levels of CXCL1, G-CSF, IL-1α, and CCL2 and an increase in the numbers of splenic phagocytes. Functionally, splenocytes from DC-depleted mice exhibited an increased bacterial killing capacity compared to splenocytes from control mice. Cellular studies further showed that this was due to an increased production of reactive oxygen species (ROS) by neutrophils. Adoptive transfer of neutrophils from DC-depleted mice into control mice prior to Ye infection reduced the bacterial load to the level of Ye-infected DC-depleted mice, suggesting that the increased number of phagocytes with additional ROS production account for the decreased bacterial load. Furthermore, after incubation with serum from DC-depleted mice splenocytes from control mice increased their bacterial killing capacity, most likely due to enhanced ROS production by neutrophils, indicating that serum factors from DC-depleted mice account for this effect. In summary, we could show that DC depletion triggers phagocyte accumulation in the spleen and enhances their anti-bacterial killing capacity upon bacterial infection.
Fil: Autenrieth, Stella E.. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; Alemania
Fil: Warnke, Philipp. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; Alemania
Fil: Wabnitz, Guido H.. Universität Heidelberg. Institut für Immunologie; Alemania
Fil: Lucero Estrada, Cecilia Stella Marys. Universidad Nacional de San Luis. Facultad de Quimica, Bioquimica y Farmacia. Area Microbiologia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; Alemania
Fil: Pasquevich, Karina Alejandra. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; Alemania
Fil: Drechsler, Doreen. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; Alemania
Fil: Gunter, Manina. Universität Tübingen. Interfakultäres Institut Für Zellbiologie; Alemania
Fil: Hochweller, Kristin. Deutsches Krebsforschungszentrum. Abteilung Molekulare Immunologie; Alemania
Fil: Novakovic, Ana. Institut Für Pharmakologie Und ToxikologieAbteilung für Pharmakologie und experimentelle Therapie, Institut für experimentelle und klinische Pharmakologie und Toxikologie, Universität Tübingen; Alemania
Fil: Beer Hammer, Sandra. Universität Tübingen; Alemania
Fil: Samstag, Yvonne. Universität Heidelberg; Alemania
Fil: Hämmerling, Günter J.. Deutsches Krebsforschungszentrum. Abteilung Molekulare Immunologie; Alemania
Fil: Garbi, Natalio. Deutsches Krebsforschungszentrum. Abteilung Molekulare Immunologie; Alemania. Universität Bonn; Alemania
Fil: Autenrieth, Ingo B.. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; Alemania
description Dendritic cells (DCs) as professional antigen-presenting cells play an important role in the initiation and modulation of the adaptive immune response. However, their role in the innate immune response against bacterial infections is not completely defined. Here we have analyzed the role of DCs and their impact on the innate anti-bacterial host defense in an experimental infection model of Yersinia enterocolitica (Ye). We used CD11c-diphtheria toxin (DT) mice to deplete DCs prior to severe infection with Ye. DC depletion significantly increased animal survival after Ye infection. The bacterial load in the spleen of DC-depleted mice was significantly lower than that of control mice throughout the infection. DC depletion was accompanied by an increase in the serum levels of CXCL1, G-CSF, IL-1α, and CCL2 and an increase in the numbers of splenic phagocytes. Functionally, splenocytes from DC-depleted mice exhibited an increased bacterial killing capacity compared to splenocytes from control mice. Cellular studies further showed that this was due to an increased production of reactive oxygen species (ROS) by neutrophils. Adoptive transfer of neutrophils from DC-depleted mice into control mice prior to Ye infection reduced the bacterial load to the level of Ye-infected DC-depleted mice, suggesting that the increased number of phagocytes with additional ROS production account for the decreased bacterial load. Furthermore, after incubation with serum from DC-depleted mice splenocytes from control mice increased their bacterial killing capacity, most likely due to enhanced ROS production by neutrophils, indicating that serum factors from DC-depleted mice account for this effect. In summary, we could show that DC depletion triggers phagocyte accumulation in the spleen and enhances their anti-bacterial killing capacity upon bacterial infection.
publishDate 2012
dc.date.none.fl_str_mv 2012-02
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/11336/14618
Autenrieth, Stella E.; Warnke, Philipp; Wabnitz, Guido H.; Lucero Estrada, Cecilia Stella Marys; Pasquevich, Karina Alejandra; et al.; Depletion of dendritic cells enhances innate anti-bacterial host defense through modulation of phagocyte homeostasis; Public Library of Science; Plos Pathogens; 8; 2; 2-2012; 1-16
1553-7366
url http://hdl.handle.net/11336/14618
identifier_str_mv Autenrieth, Stella E.; Warnke, Philipp; Wabnitz, Guido H.; Lucero Estrada, Cecilia Stella Marys; Pasquevich, Karina Alejandra; et al.; Depletion of dendritic cells enhances innate anti-bacterial host defense through modulation of phagocyte homeostasis; Public Library of Science; Plos Pathogens; 8; 2; 2-2012; 1-16
1553-7366
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1002552
info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.ppat.1002552
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
application/pdf
dc.publisher.none.fl_str_mv Public Library of Science
publisher.none.fl_str_mv Public Library of 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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