000169757 001__ 169757
000169757 005__ 20240229133654.0
000169757 0247_ $$2doi$$a10.1016/j.ijmm.2021.151517
000169757 0247_ $$2pmid$$apmid:34233227
000169757 0247_ $$2ISSN$$a1438-4221
000169757 0247_ $$2ISSN$$a1618-0607
000169757 0247_ $$2altmetric$$aaltmetric:108940129
000169757 037__ $$aDKFZ-2021-01540
000169757 041__ $$aEnglish
000169757 082__ $$a610
000169757 1001_ $$aBieber, Kristin$$b0
000169757 245__ $$aSystemic bacterial infections affect dendritic cell development and function.
000169757 260__ $$aMünchen$$bElsevier$$c2021
000169757 3367_ $$2DRIVER$$aarticle
000169757 3367_ $$2DataCite$$aOutput Types/Journal article
000169757 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1626090482_23744
000169757 3367_ $$2BibTeX$$aARTICLE
000169757 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000169757 3367_ $$00$$2EndNote$$aJournal Article
000169757 500__ $$a#LA:F171#
000169757 520__ $$aDendritic cells (DCs) are critical in host defense against infection. DC depletion is an early event in the course of sepsis that may impair the host defense mechanisms. Here, we addressed whether DC depletion and dysfunction are pathogen-independent, mediated via pattern recognition receptors, and are due to impaired DC development upon systemic infection with the Gram-negative bacterium Escherichia coli and the Gram-positive pathogen Staphylococcus aureus. Infection with E. coli and S. aureus led to reduced numbers of splenic DC subsets and of DC progenitors in the bone marrow (BM) with this effect persisting significantly longer in mice infected with S. aureus than with E. coli. The reduction of DC subsets and their progenitors was mainly TLR-independent as was the infection-induced monopoiesis. Moreover, de novo DC development was impaired in mice infected with S. aureus, and BM cells from E. coli or S. aureus infected mice favored macrophage differentiation in vitro. As a consequence of reduced DC numbers and their reduced expression of MHC II less CD4+ and CD8+ T cells, especially Th1 and IFN-γ producing CD8+ T cells, could be detected in S. aureus compared to E. coli infected mice. These differences are reflected in the rapid killing of E. coli as opposed to an increase in bacterial load in S. aureus. In summary, our study supports the idea that systemic bacterial infections generally affect the number and development of DCs and thereby the T cell responses, but the magnitude is pathogen-dependent.
000169757 536__ $$0G:(DE-HGF)POF4-316$$a316 - Infektionen, Entzündung und Krebs (POF4-316)$$cPOF4-316$$fPOF IV$$x0
000169757 588__ $$aDataset connected to CrossRef, PubMed, , Journals: inrepo01.inet.dkfz-heidelberg.de
000169757 650_7 $$2Other$$aDendritic cells
000169757 650_7 $$2Other$$aDevelopment
000169757 650_7 $$2Other$$aEscherichia coli
000169757 650_7 $$2Other$$aInfection
000169757 650_7 $$2Other$$aInnate immune defense
000169757 650_7 $$2Other$$aMonocytes
000169757 650_7 $$2Other$$aStaphylococcus aureus
000169757 650_7 $$2Other$$aTLR
000169757 7001_ $$0P:(DE-He78)b676990c2f64e3295740d42e356fb053$$aGünter, Manina$$b1$$udkfz
000169757 7001_ $$aPasquevich, Karina A$$b2
000169757 7001_ $$0P:(DE-He78)d3dbba28fe1239effd15962787cbc363$$aAutenrieth, Stella$$b3$$eLast author$$udkfz
000169757 773__ $$0PERI:(DE-600)2020515-6$$a10.1016/j.ijmm.2021.151517$$gVol. 311, no. 6, p. 151517 -$$n6$$p151517$$tInternational journal of medical microbiology$$v311$$x1438-4221$$y2021
000169757 909CO $$ooai:inrepo02.dkfz.de:169757$$pVDB
000169757 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)b676990c2f64e3295740d42e356fb053$$aDeutsches Krebsforschungszentrum$$b1$$kDKFZ
000169757 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)d3dbba28fe1239effd15962787cbc363$$aDeutsches Krebsforschungszentrum$$b3$$kDKFZ
000169757 9130_ $$0G:(DE-HGF)POF3-316$$1G:(DE-HGF)POF3-310$$2G:(DE-HGF)POF3-300$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lKrebsforschung$$vInfections and cancer$$x0
000169757 9131_ $$0G:(DE-HGF)POF4-316$$1G:(DE-HGF)POF4-310$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lKrebsforschung$$vInfektionen, Entzündung und Krebs$$x0
000169757 9141_ $$y2021
000169757 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2021-02-02
000169757 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2021-02-02
000169757 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2021-02-02
000169757 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences$$d2021-02-02
000169757 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2021-02-02
000169757 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews$$d2021-02-02
000169757 915__ $$0StatID:(DE-HGF)1190$$2StatID$$aDBCoverage$$bBiological Abstracts$$d2021-02-02
000169757 915__ $$0StatID:(DE-HGF)0113$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2021-02-02
000169757 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2021-02-02
000169757 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bINT J MED MICROBIOL : 2019$$d2021-02-02
000169757 915__ $$0StatID:(DE-HGF)9900$$2StatID$$aIF < 5$$d2021-02-02
000169757 9201_ $$0I:(DE-He78)F171-20160331$$kF171$$lDentritische Zellen bei Infektionen und Krebs$$x0
000169757 980__ $$ajournal
000169757 980__ $$aVDB
000169757 980__ $$aI:(DE-He78)F171-20160331
000169757 980__ $$aUNRESTRICTED