Evidence map›Paper›PMID 20861832›Full record

ArticleMucosal immunology2011

Mast cell/IL-4 control of Francisella tularensis replication and host cell death is associated with increased ATP production and phagosomal acidification.

A R Rodriguez, J-J Yu, A K Murthy, M N Guentzel, K E Klose, T G Forsthuber, J P Chambers, M T Berton, B P Arulanandam

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. The immune response toFrontiers in microbiology · 2025
    Review
  2. Article
  3. Article
  4. Mast Cells Respond toFrontiers in immunology · 2018
    Article
  5. Review
  6. Article
  7. Article
  8. Mast cell function: a new vision of an old cell.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2014
    Review
  9. Article
  10. Article
  11. Mechanisms of Francisella tularensis intracellular pathogenesis.Cold Spring Harbor perspectives in medicine · 2013
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Immunity to Francisella.Frontiers in microbiology · 2011
    Article
  19. Article
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

9 authors at 3 institutions in 2 countries.

A R RodriguezDepartment of Biology, South Texas Center for Emerging Infectious Diseases, University of Texas at San Antonio, San Antonio, Texas, USA.
J-J Yu
A K Murthy
M N Guentzel
K E Klose
T G Forsthuber
J P Chambers
M T Berton
B P Arulanandam
The University of Texas at San Antonio · USTexas Center for Infectious Disease · USBipar · FR

Funding

UTSA RISE Research Training ProgramR25GM060655 · NIGMS · UNIVERSITY OF TEXAS SAN ANTONIO · PI BAREA-RODRIGUEZ, EDWIN J · 2000 to 2022
$21.6M
Tularemia: Pathogenesis and Host ResponseP01AI057986 · NIAID · UNIVERSITY OF TEXAS SAN ANTONIO · PI KLOSE, KARL E · 2005 to 2009
$6.1M
NIAID NIH HHS P01 AI057986NIGMS NIH HHS GM60655NIGMS NIH HHS R25 GM060655
6 · The paper itself

Abstract

Mast cells are now recognized as effective modulators of innate immunity. We recently reported that mast cells and secreted interleukin-4 (IL-4) effectively control intramacrophage replication of Francisella tularensis Live Vaccine Strain (LVS), and that mice deficient in mast cells or IL-4 receptor (IL-4R(-/-)) exhibit greater susceptibility to pulmonary challenge. In this study, we further evaluated the mechanism(s) by which mast cells/IL-4 control intramacrophage bacterial replication and host cell death, and found that IL-4R(-/-) mice exhibited significantly greater induction of active caspase-3 within lung macrophages than wild-type animals following intranasal challenge with either LVS or the human virulent type A strain SCHU S4. Treatment of LVS-infected bone-marrow-derived macrophages with a pancaspase inhibitor (zVAD) did not alter bacterial replication, but minimized active caspase-3 and other markers (Annexin V and propidium iodide) of cell death, whereas treatment with both rIL-4 and zVAD resulted in concomitant reduction of both parameters, suggesting that inhibition of bacterial replication by IL-4 was independent of caspase activation. Interestingly, IL-4-treated infected macrophages exhibited significantly increased ATP production and phagolysosomal acidification, as well as enhanced mannose receptor upregulation and increased internalization with acidification, which correlated with observations in mast cell-macrophage co-cultures, with resultant decreases in F. tularensis replication.

Indexed as

Francisella tularensisHost-Pathogen InteractionsAdenosine TriphosphateAnimalsCaspase 3Cell DeathCells, CulturedEnzyme ActivationEnzyme InhibitorsGene Expression RegulationInterleukin-4Lectins, C-TypeMacrophages, AlveolarMannose-Binding LectinsMannose ReceptorMast CellsAdenosine Triphosphatebenzyloxycarbonyl-valyl-alanyl-aspartic acidCaspase 3Enzyme InhibitorsInterleukin-4Lectins, C-TypeMannose-Binding LectinsMannose ReceptorOligopeptidesReceptors, Cell SurfaceReceptors, Interleukin-4

Identifiers

PMID20861832
PMCPMC3040285
OpenAlexW1986978788

What OpenQuestion holds

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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.