Evidence map›Paper›PMID 28522850›Full record

ArticleScientific reports2017

Pseudomonas aeruginosa Exolysin promotes bacterial growth in lungs, alveolar damage and bacterial dissemination.

Stéphanie Bouillot, Patrick Munro, Benoit Gallet, Emeline Reboud, François Cretin, Guillaume Golovkine, Guy Schoehn, Ina Attrée, Emmanuel Lemichez, Philippe Huber

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. 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
3.7field-weighted citation impact, top 7% 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, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Cells · 2023
    Review
  6. ExlA: A New Contributor toFrontiers in cellular and infection microbiology · 2022
    Review
  7. Neuroinflammation in neurodegenerationFrontiers in immunology · 2022
    Review
  8. Molecular Mechanisms Involved in Pseudomonas aeruginosa Bacteremia.Advances in experimental medicine and biology · 2022
    Review
  9. Review
  10. Article
  11. Pathogenesis of Gram-Negative Bacteremia.Clinical microbiology reviews · 2021
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Frontiers in cellular and infection microbiology · 2017
    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

10 authors at 2 institutions in 1 country.

Stéphanie BouillotUniversité Grenoble Alpes, F-38000, Grenoble, France.
Patrick MunroINSERM, U1065, F-06204, Grenoble, France.
Benoit GalletUniversité Grenoble Alpes, F-38000, Grenoble, France.ORCID 0000-0001-8758-7681
Emeline ReboudUniversité Grenoble Alpes, F-38000, Grenoble, France.
François CretinUniversité Grenoble Alpes, F-38000, Grenoble, France.
Guillaume GolovkineUniversité Grenoble Alpes, F-38000, Grenoble, France.
Guy SchoehnUniversité Grenoble Alpes, F-38000, Grenoble, France.
Ina AttréeUniversité Grenoble Alpes, F-38000, Grenoble, France.
Emmanuel LemichezINSERM, U1065, F-06204, Grenoble, France.
Philippe HuberUniversité Grenoble Alpes, F-38000, Grenoble, France. phuber@cea.fr.
Centre National de la Recherche Scientifique · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exolysin (ExlA) is a recently-identified pore-forming toxin secreted by a subset of Pseudomonas aeruginosa strains identified worldwide and devoid of Type III secretion system (T3SS), a major virulence factor. Here, we characterized at the ultrastructural level the lesions caused by an ExlA-secreting strain, CLJ1, in mouse infected lungs. CLJ1 induced necrotic lesions in pneumocytes and endothelial cells, resulting in alveolo-vascular barrier breakdown. Ectopic expression of ExlA in an exlA-negative strain induced similar tissue injuries. In addition, ExlA conferred on bacteria the capacity to proliferate in lungs and to disseminate in secondary organs, similar to bacteria possessing a functional T3SS. CLJ1 did not promote a strong neutrophil infiltration in the alveoli, owing to the weak pro-inflammatory cytokine reaction engendered by the strain. However, CLJ1 was rapidly eliminated from the blood in a bacteremia model, suggesting that it can be promptly phagocytosed by immune cells. Together, our study ascribes to ExlA-secreting bacteria the capacity to proliferate in the lung and to damage pulmonary tissues, thereby promoting metastatic infections, in absence of substantial immune response exacerbation.

Indexed as

Alveolar Epithelial CellsAnimalsBacteremiaBacterial ToxinsFemaleMiceMice, Inbred BALB CPhagocytosisPore Forming Cytotoxic ProteinsPseudomonas aeruginosaBacterial ToxinsPore Forming Cytotoxic Proteins

Identifiers

PMID28522850
PMCPMC5437091
OpenAlexW2613581195

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.