Evidence map›Paper›PMID 31133714›Full record

ArticleScientific reports2019

Bacterial flagellin promotes viral entry via an NF-kB and Toll Like Receptor 5 dependent pathway.

Elizabeth K Benedikz, Dalan Bailey, Charlotte N L Cook, Daniel Gonçalves-Carneiro, Michelle M C Buckner, Jessica M A Blair, Timothy J Wells, Nicola F Fletcher, Margaret Goodall, Adriana Flores-Langarica and 10 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Flagellin FromFrontiers in immunology · 2021
    Article
  14. The Role of Innate Immunity in Pulmonary Infections.BioMed research international · 2021
    Review
  15. Review
  16. Article
  17. Microbiota and Its Role on Viral Evasion: Is It With Us or Against Us?Frontiers in cellular and infection microbiology · 2019
    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

20 authors at 7 institutions in 1 country.

Elizabeth K BenedikzInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK.
Dalan BaileyInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK.
Charlotte N L CookInstitute of Microbiology and Infection, University of Birmingham, Birmingham, UK.
Daniel Gonçalves-CarneiroInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK.ORCID http://orcid.org/0000-0002-9333-1540
Michelle M C BucknerInstitute of Microbiology and Infection, University of Birmingham, Birmingham, UK.ORCID http://orcid.org/0000-0001-9884-2318
Jessica M A BlairInstitute of Microbiology and Infection, University of Birmingham, Birmingham, UK.
Timothy J WellsInstitute of Microbiology and Infection, University of Birmingham, Birmingham, UK.
Nicola F FletcherInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK.
Margaret GoodallInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK.ORCID http://orcid.org/0000-0003-0177-684X
Adriana Flores-LangaricaInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK.
Robert A KingsleyInstitute of Food Research, Norwich, UK.
Jens MadsenDepartment of Child Health, University of Southampton, Southampton, UK.
Jessica TeelingBiological Sciences, University Hospital Southampton NHS Foundation Trust, Southampton, UK.ORCID http://orcid.org/0000-0003-4004-7391
Sebastian L JohnstonNational Heart and Lung Institute, Imperial College London, London, UK.ORCID http://orcid.org/0000-0003-3009-9200
Calman A MacLennanJenner Institute, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Peter BalfeInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK.ORCID http://orcid.org/0000-0002-6246-0876
Ian R HendersonInstitute of Microbiology and Infection, University of Birmingham, Birmingham, UK.
Laura J V PiddockInstitute of Microbiology and Infection, University of Birmingham, Birmingham, UK.ORCID http://orcid.org/0000-0003-1460-473X
Adam F CunninghamInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK.
Jane A McKeatingInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK. jane.mckeating@ndm.ox.ac.uk.ORCID http://orcid.org/0000-0002-7229-5886
University of Birmingham · GBUniversity of Oxford · GBImperial College London · GBQuadram Institute · GBThe Pirbright Institute · GBUniversity Hospital Southampton NHS Foundation Trust · GBUniversity of Southampton · GB

Funding

Biotechnology and Biological Sciences Research Council BB/L009986/1Biotechnology and Biological Sciences Research Council BBS/E/I/00007034Medical Research Council G0400802Medical Research Council G0801976Medical Research Council G1100247Medical Research Council MR/P008852/1Medical Research Council MR/P021735/1Medical Research Council MR/R022011/1Wellcome TrustWellcome Trust (Wellcome) IA 200838/Z/16/Z
6 · The paper itself

Abstract

Viruses and bacteria colonize hosts by invading epithelial barriers. Recent studies have shown that interactions between the microbiota, pathogens and the host can potentiate infection through poorly understood mechanisms. Here, we investigated whether diverse bacterial species could modulate virus internalization into host cells, often a rate-limiting step in establishing infections. Lentiviral pseudoviruses expressing influenza, measles, Ebola, Lassa or vesicular stomatitis virus envelope glycoproteins enabled us to study entry of viruses that exploit diverse internalization pathways. Salmonella Typhimurium, Escherichia coli and Pseudomonas aeruginosa significantly increased viral uptake, even at low bacterial frequencies. This did not require bacterial contact with or invasion of host cells. Studies determined that the bacterial antigen responsible for this pro-viral activity was the Toll-Like Receptor 5 (TLR5) agonist flagellin. Exposure to flagellin increased virus attachment to epithelial cells in a temperature-dependent manner via TLR5-dependent activation of NF-ΚB. Importantly, this phenotype was both long lasting and detectable at low multiplicities of infection. Flagellin is shed from bacteria and our studies uncover a new bystander role for this protein in regulating virus entry. This highlights a new aspect of viral-bacterial interplay with significant implications for our understanding of polymicrobial-associated pathogenesis.

Indexed as

Virus InternalizationA549 CellsAntigens, BacterialBacterial InfectionsCoinfectionDisease SusceptibilityEpithelial CellsFlagellinGene Knockdown TechniquesHEK293 CellsHost Microbial InteractionsHumansLungPermeabilityRNA, Small InterferingSignal TransductionAntigens, BacterialFlagellinRELA protein, humanRNA, Small InterferingTLR5 protein, humanToll-Like Receptor 5Transcription Factor RelA

Identifiers

PMID31133714
PMCPMC6536546
OpenAlexW2946798968

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.