Evidence map›Paper›PMID 28684793›Full record

ArticleScientific reports2017

Differentiating Staphylococcus aureus from Escherichia coli mastitis: S. aureus triggers unbalanced immune-dampening and host cell invasion immediately after udder infection.

Juliane Günther, Wolfram Petzl, Isabel Bauer, Siriluck Ponsuksili, Holm Zerbe, Hans-Joachim Schuberth, Ronald M Brunner, Hans-Martin Seyfert

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
11.5field-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

57 citing papers in PubMed, 112 citations in OpenAlex.

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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 4 institutions in 1 country.

Juliane GüntherInstitute for Genome Biology, Leibniz Institute for Farm Animal Biology, 18196, Dummerstorf, Germany.
Wolfram PetzlClinic for Ruminants with Ambulance and Herd Health Services, Centre for Clinical Veterinary Medicine, Ludwig-Maximilians-University Munich, 85764, Oberschleißheim, Germany.
Isabel BauerInstitute for Genome Biology, Leibniz Institute for Farm Animal Biology, 18196, Dummerstorf, Germany.
Siriluck PonsuksiliInstitute for Genome Biology, Leibniz Institute for Farm Animal Biology, 18196, Dummerstorf, Germany.
Holm ZerbeClinic for Ruminants with Ambulance and Herd Health Services, Centre for Clinical Veterinary Medicine, Ludwig-Maximilians-University Munich, 85764, Oberschleißheim, Germany.
Hans-Joachim SchuberthImmunology Unit, University of Veterinary Medicine Foundation, 30173, Hannover, Germany.
Ronald M BrunnerInstitute for Genome Biology, Leibniz Institute for Farm Animal Biology, 18196, Dummerstorf, Germany.
Hans-Martin SeyfertInstitute for Genome Biology, Leibniz Institute for Farm Animal Biology, 18196, Dummerstorf, Germany. seyfert@fbn-dummerstorf.de.
Research Institute for Farm Animal Biology (FBN) · DEInstitute of Bioinformatics and Systems Biology · DELudwig-Maximilians-Universität München · DEUniversity of Veterinary Medicine Hannover, Foundation · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The etiology determines quality and extent of the immune response after udder infection (mastitis). Infections with Gram negative bacteria (e.g. Escherichia coli) will quickly elicit strong inflammation of the udder, fully activate its immune defence via pathogen receptor driven activation of IκB/NF-κB signaling. This often eradicates the pathogen. In contrast, Gram-positive bacteria (e.g. Staphylococcus aureus) will slowly elicit a much weaker inflammation and immune response, frequently resulting in chronic infections. However, it was unclear which immune regulatory pathways are specifically triggered by S. aureus causing this partial immune subversion. We therefore compared in first lactating cows the earliest (1-3 h) udder responses against infection with mastitis causing pathogens of either species. Global transcriptome profiling, bioinformatics analysis and experimental validation of key aspects revealed as S. aureus infection specific features the (i) failure to activating IκB/NF-κB signaling; (ii) activation of the wnt/β-catenin cascade resulting in active suppression of NF-κB signaling and (iii) rearrangement of the actin-cytoskeleton through modulating Rho GTPase regulated pathways. This facilitates invasion of pathogens into host cells. Hence, S. aureus mastitis is characterized by eliciting unbalanced immune suppression rather than inflammation and invasion of S. aureus into the epithelial cells of the host causing sustained infection.

Indexed as

Host-Pathogen InteractionsActin CytoskeletonAnimalsbeta CateninCattleEpithelial CellsEscherichia coliEscherichia coli InfectionsFemaleGene Expression ProfilingGene Expression RegulationImmunity, InnateMammary Glands, AnimalMastitis, BovineNF-kappa BNF-KappaB Inhibitor alphabeta CateninNF-kappa BNF-KappaB Inhibitor alpharho GTP-Binding ProteinsWnt Proteins

Identifiers

PMID28684793
PMCPMC5500526
OpenAlexW2733861029

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.