Evidence map›Paper›PMID 28381209›Full record

ArticleBMC microbiology2017

Supplemental invasion of Salmonella from the perspective of Salmonella enterica serovars Kentucky and Typhimurium.

Kevin Howe, Sanaz Salehi, R Hartford Bailey, John P Brooks, Robert Wills, Mark L Lawrence, Attila Karsi

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Nanozymes Integrated Biochips Toward Smart Detection System.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  2. Multilocus sequence typing of multidrug-resistant Salmonella strains circulating in poultry farms of Bangladesh.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2021
    Article
  3. Article
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

7 authors.

Kevin HoweDepartment of Pathobiology and Population Medicine, College of Veterinary Medicine, Mississippi State University, Mississippi State, Mississippi State, MS, USA.
Sanaz SalehiDepartment of Pathobiology and Population Medicine, College of Veterinary Medicine, Mississippi State University, Mississippi State, Mississippi State, MS, USA.
R Hartford BaileyDepartment of Pathobiology and Population Medicine, College of Veterinary Medicine, Mississippi State University, Mississippi State, Mississippi State, MS, USA. rhbailey@cvm.msstate.edu.
John P BrooksUSDA-ARS, Genetics and Precision Agriculture Unit, Mississippi State, MS, USA.
Robert WillsDepartment of Pathobiology and Population Medicine, College of Veterinary Medicine, Mississippi State University, Mississippi State, Mississippi State, MS, USA.
Mark L LawrenceDepartment of Basic Sciences, College of Veterinary Medicine, Mississippi State University, Mississippi State, MS, USA.
Attila KarsiDepartment of Basic Sciences, College of Veterinary Medicine, Mississippi State University, Mississippi State, MS, USA. karsi@cvm.msstate.edu.ORCID 0000-0001-6845-3346

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCritical to the development of Salmonellosis in humans is the interaction of the bacterium with the epithelial lining of the gastrointestinal tract. Traditional scientific reasoning held type III secretion system (T3SS) as the virulence factor responsible for bacterial invasion. In this study, field-isolated Salmonella enterica serovar Kentucky and a known human pathogen Salmonella enterica serovar Typhimurium were mutated and evaluated for the invasion of human colorectal adenocarcinoma epithelial cells.

resultsS. enterica serovar Kentucky was shown to actively invade a eukaryotic monolayer, though at a rate that was significantly lower than Typhimurium. Additionally, strains mutated for T3SS formation were less invasive than the wild-type strains, but the decrease in invasion was not significant in Kentucky.

conclusionsStrains mutated for T3SS formation were able to initiate invasion of the eukaryotic monolayer to varying degrees based on strain, In the case of Kentucky, the mutated strain initiated invasion at a level that was not significantly different from the wild-type strain. A different result was observed for Typhimurium as the mutation significantly lowered the rate of invasion in comparison to the wild-type strain.

Indexed as

SerogroupCaco-2 CellsCell Culture TechniquesColony Count, MicrobialDNA, BacterialEpithelial CellsGene Expression Regulation, BacterialGenes, BacterialHumansKentuckyPhenotypeSalmonella entericaSalmonella InfectionsSalmonella typhimuriumSequence DeletionType III Secretion SystemsDNA, BacterialType III Secretion SystemsVirulence FactorsHost TropismInternalizationInvasionKentuckySalmonellaType III Secretion SystemTyphimurium

Identifiers

PMID28381209
PMCPMC5382418

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.