Evidence map›Paper›PMID 21115717›Full record

ArticleInfection and immunity2011

Comparative kinetics of Escherichia coli- and Staphylococcus aureus-specific activation of key immune pathways in mammary epithelial cells demonstrates that S. aureus elicits a delayed response dominated by interleukin-6 (IL-6) but not by IL-1A or tumor necrosis factor alpha.

Juliane Günther, Kathrin Esch, Norbert Poschadel, Wolfram Petzl, Holm Zerbe, Simone Mitterhuemer, Helmut Blum, Hans-Martin Seyfert

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
13.0field-weighted citation impact, top 1% 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

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 174 citations in OpenAlex.

  1. Pooled it
  2. A Biological Transition Around 200 × 10International journal of molecular sciences · 2026
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  6. Microbiology spectrum · 2024
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Exosomes in Mastitis-Research Status, Opportunities, and Challenges.Animals : an open access journal from MDPI · 2022
    Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Cells · 2021
    Article

21 more citing papers are in PubMed but not listed here.

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.

Juliane GüntherResearch Unit for Molecular Biology, Leibniz Institute for Farm Animal Biology, Wilhelm-Stahl-Allee 2, 18196 Dummerstorf, Germany.
Kathrin Esch
Norbert Poschadel
Wolfram Petzl
Holm Zerbe
Simone Mitterhuemer
Helmut Blum
Hans-Martin Seyfert
Ludwig-Maximilians-Universität München · DEResearch Institute for Farm Animal Biology (FBN) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infections of the udder by Escherichia coli very often elicit acute inflammation, while Staphylococcus aureus infections tend to cause mild, subclinical inflammation and persistent infections. The molecular causes underlying the different disease patterns are poorly understood. We therefore profiled the kinetics and extents of global changes in the transcriptome of primary bovine mammary epithelial cells (MEC) after challenging them with heat-inactivated preparations of E. coli or S. aureus pathogens. E. coli swiftly and strongly induced an expression of cytokines and bactericidal factors. S. aureus elicited a retarded response and failed to quickly induce an expression of bactericidal factors. Both pathogens induced similar patterns of chemokines for cell recruitment into the udder, but E. coli stimulated their synthesis much faster and stronger. The genes that are exclusively and most strongly upregulated by E. coli may be clustered into a regulatory network with tumor necrosis factor alpha (TNF-α) and interleukin-1 (IL-1) in a central position. In contrast, the expression of these master cytokines is barely regulated by S. aureus. Both pathogens quickly trigger an enhanced expression of IL-6. This is still possible after completely abrogating MyD88-dependent Toll-like receptor (TLR) signaling in MEC. The E. coli-specific strong induction of TNF-α and IL-1 expression may be causative for the severe inflammatory symptoms of animals suffering from E. coli mastitis, while the avoidance to quickly induce the synthesis of bactericidal factors may support the persistent survival of S. aureus within the udder. We suggest that S. aureus subverts the MyD88-dependent activation of immune gene expression in MEC.

Indexed as

AnimalsCattleDown-RegulationEpithelial CellsEscherichia coliFemaleGene Expression ProfilingGene Expression RegulationInterleukin-1alphaInterleukin-6Mammary Glands, AnimalMyeloid Differentiation Factor 88RNA, MessengerSignal TransductionStaphylococcus aureusTime FactorsInterleukin-1alphaInterleukin-6Myeloid Differentiation Factor 88RNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID21115717
PMCPMC3028868
OpenAlexW2114426583

What OpenQuestion holds

Textmetadata
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.