Evidence map›Paper›PMID 24319266›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

The pore-forming toxin listeriolysin O is degraded by neutrophil metalloproteinase-8 and fails to mediate Listeria monocytogenes intracellular survival in neutrophils.

Eusondia Arnett, Stephen Vadia, Colleen C Nackerman, Steve Oghumu, Abhay R Satoskar, Kenneth R McLeish, Silvia M Uriarte, Stephanie Seveau

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

  1. Article
  2. Liposomal Nanotraps NeutralizeInfectious microbes & diseases · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Genomic and pathogenicity islands ofFrontiers in molecular biosciences · 2023
    Review
  7. Review
  8. Article
  9. Article
  10. Therapeutic targeting of neutrophil exocytosis.Journal of leukocyte biology · 2020
    Review
  11. Human Neutrophil Granule Exocytosis in Response toPathogens (Basel, Switzerland) · 2020
    Article
  12. Neutrophil pyroptosis: new perspectives on sepsis.Cellular and molecular life sciences : CMLS · 2019
    Review
  13. Innate and Adaptive Immune Responses duringMicrobiology spectrum · 2019
    Article
  14. Article
  15. Article
  16. Review
  17. Listeriolysin O: from bazooka to Swiss army knife.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  18. Monocytes Are the Predominant Cell Type Associated withJournal of immunology (Baltimore, Md. : 1950) · 2017
    Article
  19. Review
  20. 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

8 authors.

Eusondia ArnettDepartment of Microbiology, The Ohio State University, Columbus, OH 43210;
Stephen Vadia
Colleen C Nackerman
Steve Oghumu
Abhay R Satoskar
Kenneth R McLeish
Silvia M Uriarte
Stephanie Seveau

Funding

Mechanism of Neutrophil ActivationI01BX001838 · VA · LOUISVILLE VA MEDICAL MEDICAL CENTER · PI MCLEISH, KENNETH R · 2013 to 2016
–
BLRD VA I01 BX001838
6 · The paper itself

Abstract

The pore-forming toxin listeriolysin O (LLO) is a major virulence factor secreted by the facultative intracellular pathogen Listeria monocytogenes. This toxin facilitates L. monocytogenes intracellular survival in macrophages and diverse nonphagocytic cells by disrupting the internalization vesicle, releasing the bacterium into its replicative niche, the cytosol. Neutrophils are innate immune cells that play an important role in the control of infections, yet it was unknown if LLO could confer a survival advantage to L. monocytogenes in neutrophils. We report that LLO can enhance the phagocytic efficiency of human neutrophils and is unable to protect L. monocytogenes from intracellular killing. To explain the absence of L. monocytogenes survival in neutrophils, we hypothesized that neutrophil degranulation leads to the release of LLO-neutralizing molecules in the forming phagosome. In support of this, L. monocytogenes is a potent inducer of neutrophil degranulation, since its virulence factors, such as LLO, facilitate granule exocytosis. Within the first few minutes of interaction with L. monocytogenes, granules can fuse with the plasma membrane at the bacterial interaction site before closure of the phagosome. Furthermore, granule products directly degrade LLO, irreversibly inhibiting its activity. The matrix metalloproteinase-8, stored in secondary granules, was identified as an endoprotease that degrades LLO, and blocking neutrophil proteases increased L. monocytogenes intracellular survival. In conclusion, we propose that LLO degradation by matrix metalloproteinase-8 during phagocytosis protects neutrophil membranes from perforation and contributes to maintaining L. monocytogenes in a bactericidal phagosome from which it cannot escape.

Indexed as

AnimalsBacterial ToxinsCell DegranulationCell LineHeat-Shock ProteinsHemolysin ProteinsHumansListeria monocytogenesMacrophagesMatrix Metalloproteinase 8MiceModels, ImmunologicalNeutrophilsPhagocytosisPhagosomesBacterial ToxinsHeat-Shock ProteinsHemolysin ProteinshlyA protein, Listeria monocytogenesMatrix Metalloproteinase 8

Identifiers

PMID24319266
PMCPMC3876913

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.