Evidence map›Paper›PMID 24708855›Full record

ArticleBMC veterinary research2014

Transcriptional approach to study porcine tracheal epithelial cells individually or dually infected with swine influenza virus and Streptococcus suis.

Yuan Dang, Claude Lachance, Yingchao Wang, Carl A Gagnon, Christian Savard, Mariela Segura, Daniel Grenier, Marcelo Gottschalk

Open access · goldAbstract read
In one paragraph

Article in BMC veterinary research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.9field-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

20 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Transcriptional Host Responses to Infection withPathogens (Basel, Switzerland) · 2023
    Article
  4. Interactions ofPathogens (Basel, Switzerland) · 2023
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  5. Application ofLife (Basel, Switzerland) · 2023
    Article
  6. Role of Metabolic Adaptation ofPathogens (Basel, Switzerland) · 2023
    Review
  7. Review
  8. Review
  9. Review
  10. Update onPathogens (Basel, Switzerland) · 2020
    Article
  11. Article
  12. Article
  13. Frontiers in microbiology · 2018
    Review
  14. Article
  15. Type I Interferon Induced byFrontiers in immunology · 2017
    Article
  16. Article
  17. Article
  18. Article
  19. Current transcriptomics in pig immunity research.Mammalian genome : official journal of the International Mammalian Genome Society · 2015
    Review
  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

8 authors at 2 institutions in 1 country.

Yuan Dang
Claude Lachance
Yingchao Wang
Carl A Gagnon
Christian Savard
Mariela Segura
Daniel Grenier
Marcelo GottschalkFaculté de Médecine Vétérinaire, Université de Montréal, 3200 Sicotte, St-Hyacinthe, J2S 2M2 Québec, Canada. marcelo.gottschalk@umontreal.ca.
Université de Montréal · CAUniversité Laval · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSwine influenza is a highly contagious viral infection in pigs affecting the respiratory tract that can have significant economic impacts. Streptococcus suis serotype 2 is one of the most important post-weaning bacterial pathogens in swine causing different infections, including pneumonia. Both pathogens are important contributors to the porcine respiratory disease complex. Outbreaks of swine influenza virus with a significant level of co-infections due to S. suis have lately been reported. In order to analyze, for the first time, the transcriptional host response of swine tracheal epithelial (NPTr) cells to H1N1 swine influenza virus (swH1N1) infection, S. suis serotype 2 infection and a dual infection, we carried out a comprehensive gene expression profiling using a microarray approach.

resultsGene clustering showed that the swH1N1 and swH1N1/S. suis infections modified the expression of genes in a similar manner. Additionally, infection of NPTr cells by S. suis alone resulted in fewer differentially expressed genes compared to mock-infected cells. However, some important genes coding for inflammatory mediators such as chemokines, interleukins, cell adhesion molecules, and eicosanoids were significantly upregulated in the presence of both pathogens compared to infection with each pathogen individually. This synergy may be the consequence, at least in part, of an increased bacterial adhesion/invasion of epithelial cells previously infected by swH1N1, as recently reported.

conclusionInfluenza virus would replicate in the respiratory epithelium and induce an inflammatory infiltrate comprised of mononuclear cells and neutrophils. In a co-infection situation, although these cells would be unable to phagocyte and kill S. suis, they are highly activated by this pathogen. S. suis is not considered a primary pulmonary pathogen, but an exacerbated production of proinflammatory mediators during a co-infection with influenza virus may be important in the pathogenesis and clinical outcome of S. suis-induced respiratory diseases.

Indexed as

Gene Expression ProfilingSwineAnimalsCell LineCoinfectionCytokinesEpithelial CellsInflammationInfluenza A Virus, H1N1 SubtypeStreptococcus suisTracheaTranscription, GeneticCytokines

Identifiers

PMID24708855
PMCPMC4022123
OpenAlexW2072966969

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.