Evidence map›Paper›PMID 33326490›Full record

ArticlePLoS pathogens2020

Bacterial behavior in human blood reveals complement evaders with some persister-like features.

Stéphane Pont, Nathan Fraikin, Yvan Caspar, Laurence Van Melderen, Ina Attrée, François Cretin

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2020. 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
1.3field-weighted citation impact, top 21% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
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  7. Article
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  9. Article
  10. Eradication ofACS infectious diseases · 2024
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  11. Review
  12. Factor H-related protein 1 promotes complement-mediated opsonization ofFrontiers in cellular and infection microbiology · 2024
    Article
  13. Role of factor H-related protein 3 inFrontiers in immunology · 2024
    Article
  14. Article
  15. Article
  16. Microorganisms · 2023
    Review
  17. Article
  18. Immune response modulation bybioRxiv : the preprint server for biology · 2023
    Article
  19. Article
  20. Molecular Mechanisms Involved in Pseudomonas aeruginosa Bacteremia.Advances in experimental medicine and biology · 2022
    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

6 authors at 3 institutions in 2 countries.

Stéphane PontUniversité Grenoble Alpes, Bacterial Pathogenesis and Cellular Responses team, CNRS ERL5261, CEA IRIG-BCI, INSERM UMR1036, Grenoble, France.ORCID 0000-0002-8142-4133
Nathan FraikinUniversité Libre de Bruxelles, Department of Molecular Biology, Cellular & Molecular Microbiology, Gosselies, Belgium.ORCID 0000-0002-0329-5313
Yvan CasparCentre Hospitalier Universitaire Grenoble Alpes, Laboratoire de bactériologie-hygiène hospitalière, Grenoble, France.ORCID 0000-0002-8332-9383
Laurence Van MelderenUniversité Libre de Bruxelles, Department of Molecular Biology, Cellular & Molecular Microbiology, Gosselies, Belgium.ORCID 0000-0002-7778-1736
Ina AttréeUniversité Grenoble Alpes, Bacterial Pathogenesis and Cellular Responses team, CNRS ERL5261, CEA IRIG-BCI, INSERM UMR1036, Grenoble, France.ORCID 0000-0002-2580-764X
François CretinUniversité Grenoble Alpes, Bacterial Pathogenesis and Cellular Responses team, CNRS ERL5261, CEA IRIG-BCI, INSERM UMR1036, Grenoble, France.ORCID 0000-0001-9939-0931
Centre National de la Recherche Scientifique · FRUniversité Libre de Bruxelles · BEInstitut polytechnique de Grenoble · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bacterial bloodstream infections (BSI) are a major health concern and can cause up to 40% mortality. Pseudomonas aeruginosa BSI is often of nosocomial origin and is associated with a particularly poor prognosis. The mechanism of bacterial persistence in blood is still largely unknown. Here, we analyzed the behavior of a cohort of clinical and laboratory Pseudomonas aeruginosa strains in human blood. In this specific environment, complement was the main defensive mechanism, acting either by direct bacterial lysis or by opsonophagocytosis, which required recognition by immune cells. We found highly variable survival rates for different strains in blood, whatever their origin, serotype, or the nature of their secreted toxins (ExoS, ExoU or ExlA) and despite their detection by immune cells. We identified and characterized a complement-tolerant subpopulation of bacterial cells that we named "evaders". Evaders shared some features with bacterial persisters, which tolerate antibiotic treatment. Notably, in bi-phasic killing curves, the evaders represented 0.1-0.001% of the initial bacterial load and displayed transient tolerance. However, the evaders are not dormant and require active metabolism to persist in blood. We detected the evaders for five other major human pathogens: Acinetobacter baumannii, Burkholderia multivorans, enteroaggregative Escherichia coli, Klebsiella pneumoniae, and Yersinia enterocolitica. Thus, the evaders could allow the pathogen to persist within the bloodstream, and may be the cause of fatal bacteremia or dissemination, in particular in the absence of effective antibiotic treatments.

Indexed as

Acinetobacter baumanniiBacteremiaBacteriaBacterial InfectionsBurkholderiaComplement ActivationComplement System ProteinsEscherichia coliHumansKlebsiella pneumoniaeMicrobial Sensitivity TestsPseudomonas aeruginosaPseudomonas InfectionsYersinia enterocoliticaComplement System Proteins

Identifiers

PMID33326490
PMCPMC7773416
OpenAlexW3110773918

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.