Evidence map›Paper›PMID 28202086›Full record

ArticleBiological research2017

Differential roles for pathogenicity islands SPI-13 and SPI-8 in the interaction of Salmonella Enteritidis and Salmonella Typhi with murine and human macrophages.

Rodrigo A Espinoza, Cecilia A Silva-Valenzuela, Fernando A Amaya, Ítalo M Urrutia, Inés Contreras, Carlos A Santiviago

Abstract read
In one paragraph

Article in Biological research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

23 citing papers in PubMed.

  1. Article
  2. Observational
  3. Article
  4. Infection biology ofEcoSal Plus · 2024
    Review
  5. Article
  6. Article
  7. Tropical medicine and infectious disease · 2023
    Review
  8. Article
  9. Prevention and Control of HumanInternational journal of food science · 2023
    Review
  10. International journal of molecular sciences · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Frontiers in microbiology · 2021
    Article
  15. TheInfection and immunity · 2020
    Article
  16. Genes · 2020
    Review
  17. Article
  18. Microorganisms · 2020
    Review
  19. Article
  20. 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

6 authors.

Rodrigo A EspinozaLaboratorio de Microbiología, Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santos Dumont 964, Independencia, Santiago, Chile.
Cecilia A Silva-ValenzuelaLaboratorio de Microbiología, Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santos Dumont 964, Independencia, Santiago, Chile.
Fernando A AmayaLaboratorio de Microbiología, Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santos Dumont 964, Independencia, Santiago, Chile.
Ítalo M UrrutiaLaboratorio de Microbiología, Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santos Dumont 964, Independencia, Santiago, Chile.
Inés ContrerasLaboratorio de Microbiología, Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santos Dumont 964, Independencia, Santiago, Chile. inescontreraso@gmail.com.
Carlos A SantiviagoLaboratorio de Microbiología, Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santos Dumont 964, Independencia, Santiago, Chile. csantiviago@ciq.uchile.cl.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSalmonella pathogenicity island (SPI)-13 is conserved in many serovars of S. enterica, including S. Enteritidis, S. Typhimurium and S. Gallinarum. However, it is absent in typhoid serovars such as S. Typhi and Paratyphi A, which carry SPI-8 at the same genomic location. Because the interaction with macrophages is a critical step in Salmonella pathogenicity, in this study we investigated the role played by SPI-13 and SPI-8 in the interaction of S. Enteritidis and S. Typhi with cultured murine (RAW264.7) and human (THP-1) macrophages.

resultsOur results showed that SPI-13 was required for internalization of S. Enteritidis in murine but not human macrophages. On the other hand, SPI-8 was not required for the interaction of S. Typhi with human or murine macrophages. Of note, the presence of an intact copy of SPI-13 in a S. Typhi mutant carrying a deletion of SPI-8 did not improve its ability to be internalized by, or survive in human or murine macrophages.

conclusionsAltogether, our results point out to different roles for SPI-13 and SPI-8 during Salmonella infection. While SPI-13 contributes to the interaction of S. Enteritidis with murine macrophages, SPI-8 is not required in the interaction of S. Typhi with murine or human macrophages. We hypothesized that typhoid serovars have lost SPI-13 and maintained SPI-8 to improve their fitness during another phase of human infection.

Indexed as

Analysis of VarianceAnimalsBacterial Physiological PhenomenaCells, CulturedCell SurvivalGenome, BacterialGenomic IslandsHumansMacrophagesMiceMicrobial InteractionsMuridaePolymerase Chain ReactionRAW 264.7 CellsSalmonella enteritidisSalmonella InfectionsEnteritidisMacrophagesRAW264.7SalmonellaSPI-13SPI-8THP-1Typhi

Identifiers

PMID28202086
PMCPMC5311848

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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.