Evidence map›Paper›PMID 19139198›Full record

ArticleInfection and immunity2009

Campylobacter jejuni drives MyD88-independent interleukin-6 secretion via Toll-like receptor 2.

Lorna M Friis, Monika Keelan, Diane E Taylor

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
9.0field-weighted citation impact, top 2% 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

31 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Campylobacter coli strains from Brazil can invade phagocytic and epithelial cells and induce IL-8 secretion.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2021
    Article
  6. Article
  7. Genes · 2020
    Article
  8. Human Immunity AgainstImmune network · 2019
    Review
  9. Article
  10. Article
  11. Article
  12. Cellular Tight Junctions Prevent EffectiveFrontiers in cellular and infection microbiology · 2018
    Article
  13. Review
  14. Article
  15. The Bacterial SpeciesFrontiers in microbiology · 2017
    Article
  16. Review
  17. Review
  18. Article
  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

3 authors at 1 institution in 1 country.

Lorna M FriisDepartment of Medical Microbiology and Immunology, University of Alberta, 1-63 Medical Sciences Building, Edmonton T6G 2H7, Alberta, Canada. lfriis@ualberta.ca
Monika Keelan
Diane E Taylor
University of Alberta · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastrointestinal disease caused by Campylobacter jejuni is characterized by localized inflammation and the destruction of the epithelial cell barrier that forms host innate protection against pathogens. This can lead to an imbalance in fluid transport across the gastrointestinal tract, resulting in severe diarrhea. The mechanisms of host cell receptor recognition of C. jejuni and downstream immune signaling pathways leading to this inflammatory disease, however, remain unclear. The aim of this study was to analyze the mechanisms involved in C. jejuni induction of the acute-phase inflammatory response regulator interleukin-6 (IL-6). Polarized intestinal epithelial Caco-2 monolayers responded to infections with Salmonella enterica serovar Typhimurium and eight isolates of C. jejuni by an increase in levels of expression and secretion of IL-6. No such IL-6 response, however, was produced upon infection with the human commensal organism Lactobacillus rhamnosus GG. The IL-6 signaling pathway was further characterized using short interfering RNA complexes to block gene expression. The inhibition of myeloid differentiation primary response protein 88 (MyD88) expression in this manner did not affect C. jejuni-induced IL-6 secretion, suggesting a MyD88-independent route to IL-6 signal transduction in C. jejuni-infected human epithelial cells. However, a significant reduction in levels of IL-6 was evident in the absence of Toll-like receptor 2 (TLR-2) expression, implying a requirement for TLR-2 in C. jejuni recognition. Caco-2 cells were also treated with heat-inactivated and purified membrane components of C. jejuni to isolate the factor responsible for triggering IL-6 signaling. The results demonstrate that C. jejuni surface polysaccharides induce IL-6 secretion from intestinal epithelial cells via TLR-2 in a MyD88-independent manner.

Indexed as

AnimalsCaco-2 CellsCampylobacter jejuniCell LineEpithelial CellsGene Expression RegulationHumansInterleukin-6IntestinesMyeloid Differentiation Factor 88Signal TransductionToll-Like Receptor 2Interleukin-6MYD88 protein, humanMyeloid Differentiation Factor 88Toll-Like Receptor 2

Identifiers

PMID19139198
PMCPMC2663148
OpenAlexW2150887383

What OpenQuestion holds

Textmetadata
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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.