Evidence map›Paper›PMID 22833676›Full record

ArticleThe Journal of biological chemistry2012

A disintegrin and metalloproteinase 17 (ADAM17) and epidermal growth factor receptor (EGFR) signaling drive the epithelial response to Staphylococcus aureus toxic shock syndrome toxin-1 (TSST-1).

Laura M Breshears, Patrick M Schlievert, Marnie L Peterson

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

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  9. Tetraspanins Function as Regulators of Cellular Signaling.Frontiers in cell and developmental biology · 2017
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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

3 authors at 2 institutions in 1 country.

Laura M BreshearsDepartment of Experimental and Clinical Pharmacology, University of Minnesota, Minneapolis, Minnesota 55455, USA.
Patrick M Schlievert
Marnie L Peterson
University of Iowa · USUniversity of Minnesota · US

Funding

Cardiotoxicity of Streptococcal Pyrogenic ExotoxinsR01AI074283 · NIAID · UNIVERSITY OF MINNESOTA · PI SCHLIEVERT, PATRICK M · 2007 to 2011
$1.6M
Staphylococcal Superantigen Interactions With Vaginal EpitheliumR01AI073366 · NIAID · UNIVERSITY OF MINNESOTA · PI PETERSON, MARNIE L · 2009 to 2012
$1.2M
NIAID NIH HHS R01 AI073366NIAID NIH HHS R01AI073366-03NIAID NIH HHS R01 AI074283NIAID NIH HHS R01AI074283
6 · The paper itself

Abstract

Staphylococcal superantigens (SAgs), such as toxic shock syndrome toxin-1 (TSST-1), are the main cause of toxic shock syndrome (TSS). SAgs deregulate the host immune system after penetrating epithelial barriers such as the vaginal mucosa. In response to TSST-1, human vaginal epithelial cells (HVECs) produce cytokines and undergo morphological changes. The epithelial signaling mechanisms employed by SAgs remain largely unknown and are the focus of the work presented here. Analysis of published microarray data identified a network of genes up-regulated by HVECs in response to TSST-1 that includes the sheddase, a disintegrin and metalloproteinase 17 (ADAM17). Investigation revealed that the ADAM17 proteolytic targets, amphiregulin (AREG), transforming growth factor α (TGFα), syndecan-1 (SDC1), and tumor necrosis factor receptor 1 (TNFR1), are shed from HVECs in response to TSST-1. TAPI-1 (an ADAM inhibitor) completely abrogates all observed shedding and the production of the cytokine interleukin-8 (IL-8). Knock-down studies show that ADAM17, but not the closely related ADAM10, is required for AREG, TGFα, and TNFR1 shedding. Both ADAM10 and ADAM17 contribute to SDC1 shedding and IL-8 production by HVECs in response to TSST-1. EGFR signaling is critical for up-regulation of IL-8 at the transcriptional level in response to TSST-1 and is also necessary for AREG, TGFα, and TNFR1 shedding. A model is proposed describing the interactions of TSST-1, ADAMs, and the EGFR that lead to establishment of a proinflammatory positive feedback loop in epithelial cells and demonstrate a role for SAgs in the initial stages of disease.

Indexed as

Models, BiologicalSignal TransductionADAM17 ProteinADAM ProteinsAmphiregulinBacterial ToxinsDipeptidesEGF Family of ProteinsEnterotoxinsErbB ReceptorsGlycoproteinsHumansHuman Umbilical Vein Endothelial CellsHydroxamic AcidsIntercellular Signaling Peptides and ProteinsInterleukin-8ADAM17 ProteinADAM17 protein, humanADAM ProteinsAmphiregulinAREG protein, humanBacterial ToxinsCXCL8 protein, humanDipeptidesEGF Family of ProteinsEGFR protein, humanenterotoxin F, StaphylococcalEnterotoxinsErbB ReceptorsGlycoproteinsHydroxamic AcidsIntercellular Signaling Peptides and ProteinsInterleukin-8N-((2-(hydroxyaminocarbonyl)methyl)-4-methylpentanoyl)-3-(2'-naphthyl)alanylalanine, 2-aminoethylamideReceptors, Tumor Necrosis Factor, Type ISDC1 protein, humanSuperantigensSyndecan-1Transforming Growth Factor alpha

Identifiers

PMID22833676
PMCPMC3463354
OpenAlexW2050122855

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.