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dc.contributor.author
Autenrieth, Stella E.
dc.contributor.author
Warnke, Philipp
dc.contributor.author
Wabnitz, Guido H.
dc.contributor.author
Lucero Estrada, Cecilia Stella Marys
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dc.contributor.author
Pasquevich, Karina Alejandra
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Drechsler, Doreen
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Gunter, Manina
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Hochweller, Kristin
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Novakovic, Ana
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Beer Hammer, Sandra
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Samstag, Yvonne
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Hämmerling, Günter J.
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Garbi, Natalio
dc.contributor.author
Autenrieth, Ingo B.
dc.date.available
2017-03-31T18:49:04Z
dc.date.issued
2012-02
dc.identifier.citation
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
dc.identifier.issn
1553-7366
dc.identifier.uri
http://hdl.handle.net/11336/14618
dc.description.abstract
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.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Public Library of Science
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Dendritic Cells
dc.subject
Phagocites
dc.subject.classification
Biología Celular, Microbiología
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dc.subject.classification
Ciencias Biológicas
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dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
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dc.title
Depletion of dendritic cells enhances innate anti-bacterial host defense through modulation of phagocyte homeostasis
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2016-11-24T19:24:20Z
dc.journal.volume
8
dc.journal.number
2
dc.journal.pagination
1-16
dc.journal.pais
Estados Unidos
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dc.journal.ciudad
San Francisco
dc.description.fil
Fil: Autenrieth, Stella E.. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; Alemania
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Fil: Warnke, Philipp. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; Alemania
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Fil: Wabnitz, Guido H.. Universität Heidelberg. Institut für Immunologie; Alemania
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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
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Fil: Pasquevich, Karina Alejandra. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; Alemania
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Fil: Drechsler, Doreen. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; Alemania
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Fil: Gunter, Manina. Universität Tübingen. Interfakultäres Institut Für Zellbiologie; Alemania
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Fil: Hochweller, Kristin. Deutsches Krebsforschungszentrum. Abteilung Molekulare Immunologie; Alemania
dc.description.fil
Fil: Novakovic, Ana. Institut Für Pharmakologie Und ToxikologieAbteilung für Pharmakologie und experimentelle Therapie, Institut für experimentelle und klinische
Pharmakologie und Toxikologie, Universität Tübingen; Alemania
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Fil: Beer Hammer, Sandra. Universität Tübingen; Alemania
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Fil: Samstag, Yvonne. Universität Heidelberg; Alemania
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Fil: Hämmerling, Günter J.. Deutsches Krebsforschungszentrum. Abteilung Molekulare Immunologie; Alemania
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Fil: Garbi, Natalio. Deutsches Krebsforschungszentrum. Abteilung Molekulare Immunologie; Alemania. Universität Bonn; Alemania
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Fil: Autenrieth, Ingo B.. Universität Tübingen. Interfakultäres Institut für Mikrobiologie und Infektionsmedizin; Alemania
dc.journal.title
Plos Pathogens
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1002552
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1371/journal.ppat.1002552
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