Evidence map›Paper›PMID 24779413›Full record

ArticleCellular microbiology2014

The focal complex of epithelial cells provides a signalling platform for interleukin-8 induction in response to bacterial pathogens.

Tyson P Eucker, Derrick R Samuelson, Mary Hunzicker-Dunn, Michael E Konkel

Open access · bronzeAbstract read
In one paragraph

Article in Cellular microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Polish journal of microbiology · 2021
    Article
  6. Article
  7. Article
  8. Article
  9. Taking Control:Frontiers in microbiology · 2020
    Review
  10. Frontiers in microbiology · 2019
    Article
  11. Article
  12. 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

4 authors at 1 institution in 1 country.

Tyson P EuckerSchool of Molecular Biosciences, College of Veterinary Medicine, Washington State University, Pullman, WA, 99164-7520, USA.
Derrick R Samuelson
Mary Hunzicker-Dunn
Michael E Konkel
Washington State University · US

Funding

TRAINING IN BIOTECHNOLOGY: EMPHASIS ON PROTEIN CHEMISTRYT32GM008336 · NIGMS · WASHINGTON STATE UNIVERSITY · PI CALL, DOUGLAS R. · 1989 to 2023
$8.9M
Molecular Bioscience Graduate Training ProgramT32GM083864 · NIGMS · WASHINGTON STATE UNIVERSITY · PI NILSON, JOHN H. · 2010 to 2014
$646k
Molecular mechanisms underlying Campylobacter jejuni cellular invasionR56AI088518 · NIAID · WASHINGTON STATE UNIVERSITY · PI KONKEL, MICHAEL E · 2011 to 2011
$324k
NIAID NIH HHS R56 AI088518NIAID NIH HHS R56 AI088518-01A1NIGMS NIH HHS T32 GM008336NIGMS NIH HHS T32 GM083864
6 · The paper itself

Abstract

Bacterial pathogens can induce an inflammatory response from epithelial tissues due to secretion of the pro-inflammatory chemokine interleukin-8 (IL-8). Many bacterial pathogens manipulate components of the focal complex (FC) to induce signalling events in host cells. We examined the interaction of several bacterial pathogens with host cells, including Campylobacter jejuni, to determine if the FC is required for induction of chemokine signalling in response to bacterial pathogens. Our data indicate that secretion of IL-8 is triggered by C. jejuni, Helicobacter pylori and Salmonella enterica serovar Typhimurium in response to engagement of β1 integrins. Additionally, we found that the secretion of IL-8 from C. jejuni infected epithelial cells requires FAK, Src and paxillin, which in turn are necessary for Erk 1/2 recruitment and activation. Targeting the FC component paxillin with siRNA prevented IL-8 secretion from cells infected with several bacterial pathogens, including C. jejuni, Helicobacter pylori, Salmonella enterica serovar Typhimurium, Staphylococcus aureus, Pseudomonas aeruginosa, and Vibrio parahaemolyticus. Our findings indicate that maximal IL-8 secretion from epithelial cells in response to bacterial infection is dependent on the FC. Based on the commonality of the host response to bacterial pathogens, we propose that the FC is a signalling platform for an epithelial cell response to pathogenic organisms.

Indexed as

Caco-2 CellsCampylobacter jejuniCell LineEpithelial CellsGram-Negative Bacterial InfectionsHelicobacter pyloriHumansIntegrin beta ChainsInterleukin-8Staphylococcus aureusIntegrin beta ChainsInterleukin-8

Identifiers

PMID24779413
PMCPMC4146656
OpenAlexW1855872860

What OpenQuestion holds

Textmetadata
LicenceTDM
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.