PMID- 22383883
OWN - NLM
STAT- MEDLINE
DCOM- 20120710
LR  - 20211021
IS  - 1553-7374 (Electronic)
IS  - 1553-7366 (Print)
IS  - 1553-7366 (Linking)
VI  - 8
IP  - 2
DP  - 2012 Feb
TI  - Depletion of dendritic cells enhances innate anti-bacterial host defense through 
      modulation of phagocyte homeostasis.
PG  - e1002552
LID - 10.1371/journal.ppat.1002552 [doi]
LID - e1002552
AB  - 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-1alpha, 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.
FAU - Autenrieth, Stella E
AU  - Autenrieth SE
AD  - Interfakultares Institut fur Mikrobiologie und Infektionsmedizin, Universitat 
      Tubingen, Tubingen, Germany. Stella.Autenrieth@medizin.uni-tuebingen.de
FAU - Warnke, Philipp
AU  - Warnke P
FAU - Wabnitz, Guido H
AU  - Wabnitz GH
FAU - Lucero Estrada, Cecilia
AU  - Lucero Estrada C
FAU - Pasquevich, Karina A
AU  - Pasquevich KA
FAU - Drechsler, Doreen
AU  - Drechsler D
FAU - Gunter, Manina
AU  - Gunter M
FAU - Hochweller, Kristin
AU  - Hochweller K
FAU - Novakovic, Ana
AU  - Novakovic A
FAU - Beer-Hammer, Sandra
AU  - Beer-Hammer S
FAU - Samstag, Yvonne
AU  - Samstag Y
FAU - Hammerling, Gunter J
AU  - Hammerling GJ
FAU - Garbi, Natalio
AU  - Garbi N
FAU - Autenrieth, Ingo B
AU  - Autenrieth IB
LA  - eng
PT  - Evaluation Study
PT  - Journal Article
DEP - 20120223
PL  - United States
TA  - PLoS Pathog
JT  - PLoS pathogens
JID - 101238921
SB  - IM
MH  - Adoptive Transfer
MH  - Animals
MH  - Bacteria/immunology
MH  - Cell Separation
MH  - Cells, Cultured
MH  - Dendritic Cells/*pathology
MH  - Female
MH  - Homeostasis/immunology
MH  - Immunity, Innate/*physiology
MH  - Mice
MH  - Mice, Transgenic
MH  - Neutrophils/transplantation
MH  - Phagocytes/immunology/*physiology
MH  - Up-Regulation/immunology
MH  - Yersinia Infections/*immunology/pathology/therapy
MH  - Yersinia enterocolitica/*immunology
PMC - PMC3285606
COIS- The authors have declared that no competing interests exist.
EDAT- 2012/03/03 06:00
MHDA- 2012/07/11 06:00
PMCR- 2012/02/23
CRDT- 2012/03/03 06:00
PHST- 2011/09/14 00:00 [received]
PHST- 2012/01/11 00:00 [accepted]
PHST- 2012/03/03 06:00 [entrez]
PHST- 2012/03/03 06:00 [pubmed]
PHST- 2012/07/11 06:00 [medline]
PHST- 2012/02/23 00:00 [pmc-release]
AID - PPATHOGENS-D-11-02080 [pii]
AID - 10.1371/journal.ppat.1002552 [doi]
PST - ppublish
SO  - PLoS Pathog. 2012 Feb;8(2):e1002552. doi: 10.1371/journal.ppat.1002552. Epub 2012 
      Feb 23.