Evidence map›Paper›PMID 25609312›Full record

ArticleScientific reports2015

The Hd, Hj, and Hz66 flagella variants of Salmonella enterica serovar Typhi modify host responses and cellular interactions.

Fernanda Schreiber, Sally Kay, Gad Frankel, Simon Clare, David Goulding, Esther van de Vosse, Jaap T van Dissel, Richard Strugnell, Guy Thwaites, Robert A Kingsley and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

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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

12 authors at 7 institutions in 4 countries.

Fernanda SchreiberThe Wellcome Trust Sanger Institute, Hinxton, Cambridge, United Kingdom.
Sally KayThe Wellcome Trust Sanger Institute, Hinxton, Cambridge, United Kingdom.
Gad FrankelCentre for Molecular Microbiology and Infection, Imperial College, London, United Kingdom.
Simon ClareThe Wellcome Trust Sanger Institute, Hinxton, Cambridge, United Kingdom.
David GouldingThe Wellcome Trust Sanger Institute, Hinxton, Cambridge, United Kingdom.
Esther van de VosseDepartment of Infectious Diseases, Leiden University Medical Center, Leiden, the Netherlands.
Jaap T van DisselDepartment of Infectious Diseases, Leiden University Medical Center, Leiden, the Netherlands.
Richard StrugnellDepartment of Microbiology and Immunology, University of Melbourne, Parkville, Australia.
Guy Thwaites1] The Hospital for Tropical Diseases, Wellcome Trust Major Overseas Programme, Oxford University Clinical Research Unit, Ho Chi Minh City, Vietnam [2] Centre for Tropical Medicine, Nuffield Department of Clinical Medicine, Oxford University, United Kingdom.
Robert A KingsleyInstitute for Food Research, Norwich, United Kingdom.
Gordon DouganThe Wellcome Trust Sanger Institute, Hinxton, Cambridge, United Kingdom.
Stephen Baker1] The Hospital for Tropical Diseases, Wellcome Trust Major Overseas Programme, Oxford University Clinical Research Unit, Ho Chi Minh City, Vietnam [2] Centre for Tropical Medicine, Nuffield Department of Clinical Medicine, Oxford University, United Kingdom [3] The London School of Hygiene and Tropical Medicine, London, United Kingdom.
Wellcome Sanger Institute · GBLeiden University Medical Center · NLHospital for Tropical Diseases · VNImperial College London · GBNuffield Orthopaedic Centre · GBQuadram Institute · GBUniversity of Melbourne · AU

Funding

Medical Research Council MR/J006874/1Wellcome Trust 089276Wellcome Trust 100087Wellcome Trust 100087/Z/12/Z
6 · The paper itself

Abstract

Salmonella Typhi, the causative agent of typhoid fever, is a monophyletic, human-restricted bacterium that exhibits limited phenotypic variation. S. Typhi from Indonesia are a notable exception, with circulating strains expressing diverse flagella antigens including Hj, Hd and Hz66. Hypothesizing that S. Typhi flagella plays a key role during infection, we constructed an S. Typhi fliC mutant and otherwise isogenic S. Typhi strains expressing the Hj, Hd, Hz66 flagella antigens. Phenotyping revealed differences in flagellum structure, strain motility and immunogenicity, but not in the ability of flagellated isolates to induce TLR5 activity. Invasion assays using epithelial and macrophage cell lines revealed differences in the ability of these S. Typhi derivatives to invade cells or induce cellular restructuring in the form of ruffles. Notably, the Hj variant induced substantial ruffles that were not fully dependent on the GTPases that contribute to this process. These data highlight important differences in the phenotypic properties of S. Typhi flagella variation and how they impact on the pathogenesis of S. Typhi.

Indexed as

Antigens, BacterialBacterial AdhesionCell CommunicationFlagellaGene Expression Regulation, BacterialHost-Pathogen InteractionsHumansIndonesiaMacrophagesSalmonella typhiTyphoid FeverAntigens, Bacterial

Identifiers

PMID25609312
PMCPMC4302301
OpenAlexW2079752663

What OpenQuestion holds

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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.