Evidence map›Paper›PMID 22383883›Full record

ArticlePLoS pathogens2012

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

Stella E Autenrieth, Philipp Warnke, Guido H Wabnitz, Cecilia Lucero Estrada, Karina A Pasquevich, Doreen Drechsler, Manina Günter, Kristin Hochweller, Ana Novakovic, Sandra Beer-Hammer and 4 more

Open access · goldAbstract readEvaluation Study
In one paragraph

Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.2field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Unraveling neutrophil-F1000Research · 2019
    Review
  8. Article
  9. Article
  10. Tumor-Resident Dendritic Cells and Macrophages Modulate the Accumulation of TCR-Engineered T Cells in Melanoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2018
    Article
  11. Article
  12. LangerinFrontiers in immunology · 2018
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 1 country.

Stella E AutenriethInterfakultäres Institut für Mikrobiologie und Infektionsmedizin, Universität Tübingen, Tübingen, Germany. Stella.Autenrieth@medizin.uni-tuebingen.de
Philipp Warnke
Guido H Wabnitz
Cecilia Lucero Estrada
Karina A Pasquevich
Doreen Drechsler
Manina Günter
Kristin Hochweller
Ana Novakovic
Sandra Beer-Hammer
Yvonne Samstag
Günter J Hämmerling
Natalio Garbi
Ingo B Autenrieth
University of Tübingen · DEHeidelberg University · DEGerman Cancer Research Center · DEUniversitätsklinikum Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Adoptive TransferAnimalsBacteriaCells, CulturedCell SeparationDendritic CellsFemaleHomeostasisImmunity, InnateMiceMice, TransgenicNeutrophilsPhagocytesUp-RegulationYersinia enterocoliticaYersinia Infections

Identifiers

PMID22383883
PMCPMC3285606
OpenAlexW2070467944

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.