Evidence map›Paper›PMID 28704569›Full record

ArticlePLoS pathogens2017

A virulence-associated filamentous bacteriophage of Neisseria meningitidis increases host-cell colonisation.

Emmanuelle Bille, Julie Meyer, Anne Jamet, Daniel Euphrasie, Jean-Philippe Barnier, Terry Brissac, Anna Larsen, Philippe Pelissier, Xavier Nassif

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

54 citing papers in PubMed, 80 citations in OpenAlex.

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  13. Structure of the virulence-associatedProceedings of the National Academy of Sciences of the United States of America · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Emmanuelle BilleInstitut Necker-Enfants Malades, INSERM U1151, CNRS UMR 8253, Paris, France.ORCID http://orcid.org/0000-0001-9172-0510
Julie MeyerInstitut Necker-Enfants Malades, INSERM U1151, CNRS UMR 8253, Paris, France.ORCID http://orcid.org/0000-0002-6144-927X
Anne JametInstitut Necker-Enfants Malades, INSERM U1151, CNRS UMR 8253, Paris, France.
Daniel EuphrasieInstitut Necker-Enfants Malades, INSERM U1151, CNRS UMR 8253, Paris, France.
Jean-Philippe BarnierInstitut Necker-Enfants Malades, INSERM U1151, CNRS UMR 8253, Paris, France.ORCID http://orcid.org/0000-0002-0603-6755
Terry BrissacInstitut Necker-Enfants Malades, INSERM U1151, CNRS UMR 8253, Paris, France.ORCID http://orcid.org/0000-0002-2549-4479
Anna LarsenInstitut Necker-Enfants Malades, INSERM U1151, CNRS UMR 8253, Paris, France.ORCID http://orcid.org/0000-0001-6681-4099
Philippe PelissierService de Chirurgie Reconstructrice et Plastique, Fondation Hôpital Saint Joseph, Paris, France.
Xavier NassifInstitut Necker-Enfants Malades, INSERM U1151, CNRS UMR 8253, Paris, France.
Délégation Paris 5 · FRHôpital Saint Joseph · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neisseria meningitidis is a commensal of human nasopharynx. In some circumstances, this bacteria can invade the bloodstream and, after crossing the blood brain barrier, the meninges. A filamentous phage, designated MDAΦ for Meningococcal Disease Associated, has been associated with invasive disease. In this work we show that the prophage is not associated with a higher virulence during the bloodstream phase of the disease. However, looking at the interaction of N. meningitidis with epithelial cells, a step essential for colonization of the nasopharynx, we demonstrate that the presence of the prophage, via the production of viruses, increases colonization of encapsulated meningococci onto monolayers of epithelial cells. The analysis of the biomass covering the epithelial cells revealed that meningococci are bound to the apical surface of host cells by few layers of heavily piliated bacteria, whereas, in the upper layers, bacteria are non-piliated but surrounded by phage particles which (i) form bundles of filaments, and/or (ii) are in some places associated with bacteria. The latter are likely to correspond to growing bacteriophages during their extrusion through the outer membrane. These data suggest that, as the biomass increases, the loss of piliation in the upper layers of the biomass does not allow type IV pilus bacterial aggregation, but is compensated by a large production of phage particles that promote bacterial aggregation via the formation of bundles of phage filaments linked to the bacterial cell walls. We propose that MDAΦ by increasing bacterial colonization in the mucosa at the site-of-entry, increase the occurrence of diseases.

Indexed as

AnimalsBacterial AdhesionEpithelial CellsFemaleFimbriae, BacterialHumansInovirusMeningococcal InfectionsMiceMice, SCIDNasopharynxNeisseria meningitidisProphagesVirulence

Identifiers

PMID28704569
PMCPMC5526601
OpenAlexW2736238444

What OpenQuestion holds

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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.