Evidence map›Paper›PMID 25114115›Full record

ArticleInfection and immunity2014

New insights into the antimicrobial effect of mast cells against Enterococcus faecalis.

Matthias Scheb-Wetzel, Manfred Rohde, Alicia Bravo, Oliver Goldmann

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 35 citations in OpenAlex.

  1. Vancomycin-Resistant, ThermotolerantFoods (Basel, Switzerland) · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Extracellular traps and the role in thrombosis.Frontiers in cardiovascular medicine · 2022
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Frontiers in immunology · 2018
    Article
  15. Group AFrontiers in immunology · 2018
    Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review
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

4 authors at 2 institutions in 2 countries.

Matthias Scheb-WetzelInfection Immunology Research Group, Helmholtz Center for Infection Research, Braunschweig, Germany.
Manfred RohdeCentral Facility for Microscopy, Helmholtz Center for Infection Research, Braunschweig, Germany.
Alicia BravoCentro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas, Madrid, Spain.
Oliver GoldmannInfection Immunology Research Group, Helmholtz Center for Infection Research, Braunschweig, Germany oliver.goldmann@helmholtz-hzi.de.
Helmholtz Centre for Infection Research · DECentro de Investigaciones Biológicas Margarita Salas · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enterococcus faecalis has emerged as an important cause of life-threatening multidrug-resistant bacterial infections in the hospital setting. The pathogenesis of enterococcal infections has remained a relatively neglected field despite their obvious clinical relevance. The objective of this study was to characterize the interactions between mast cells (MCs), an innate immune cell population abundant in the intestinal lamina propria, and E. faecalis. This study was conducted with primary bone marrow-derived murine MCs. The results demonstrated that MCs exerted an antimicrobial effect against E. faecalis that was mediated both by degranulation, with the concomitant discharge of the antimicrobial effectors contained in the granules, and by the release of extracellular traps, in which E. faecalis was snared and killed. In particular, the cathelicidin LL-37 released by the MCs had potent antimicrobial effect against E. faecalis. We also investigated the specific receptors involved in the recognition of E. faecalis by MCs. We found that Toll-like receptors (TLRs) are critically involved in the MC recognition of E. faecalis, since MCs deficient in the expression of MyD88, an adaptor molecule required for signaling by most TLRs, were significantly impaired in their capacity to degranulate, to reduce E. faecalis growth as well as to release tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) after encountering this pathogen. Furthermore, TLR2 was identified as the most prominent TLR involved in the recognition of E. faecalis by MCs. The results of this study indicate that MCs may be important contributors to the host innate immune defenses against E. faecalis.

Indexed as

AnimalsBacterial AdhesionBone Marrow CellsCells, CulturedEnterococcus faecalisGram-Positive Bacterial InfectionsMast CellsMiceMice, Inbred C57BLMice, KnockoutSignal TransductionSpecific Pathogen-Free OrganismsToll-Like Receptor 2Tlr2 protein, mouseToll-Like Receptor 2

Identifiers

PMID25114115
PMCPMC4249337
OpenAlexW2156989569

What OpenQuestion holds

Textmetadata
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.