Evidence map›Paper›PMID 26126119›Full record

ArticlePloS one2015

The Sbi Protein Contributes to Staphylococcus aureus Inflammatory Response during Systemic Infection.

Cintia Daniela Gonzalez, Camila Ledo, Constanza Giai, Ailin Garófalo, Marisa I Gómez

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

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  11. Frontiers in immunology · 2018
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  12. Epic Immune Battles of History: Neutrophils vs.Frontiers in cellular and infection microbiology · 2017
    Review
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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

5 authors at 2 institutions in 1 country.

Cintia Daniela GonzalezInstituto de Investigaciones en Microbiología y Parasitología Médica (IMPaM), Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina.
Camila LedoDepartamento de Microbiología, Parasitología e Immunología, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina.
Constanza GiaiInstituto de Investigaciones en Microbiología y Parasitología Médica (IMPaM), Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina.
Ailin GarófaloInstituto de Investigaciones en Microbiología y Parasitología Médica (IMPaM), Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina.
Marisa I GómezInstituto de Investigaciones en Microbiología y Parasitología Médica (IMPaM), Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina; Departamento de Microbiología, Parasitología e Immunología, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARUniversity of Buenos Aires · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Staphylococcus aureus is an important human pathogen that causes infections that may present high morbidity and mortality. Among its many virulence factors protein A (SpA) and Staphylococcal binding immunoglobulin protein (Sbi) bind the Fc portion of IgG interfering with opsonophagocytosis. We have previously demonstrated that SpA interacts with the TNF-α receptor (TNFR) 1 through each of the five IgG binding domains and induces the production of pro-inflammatory cytokines and chemokines. The IgG binding domains of Sbi are homologous to those of SpA, which allow us to hypothesize that Sbi might also have a role in the inflammatory response induced by S. aureus. We demonstrate that Sbi is a novel factor that participates in the induction of the inflammatory response during staphylococcal infections via TNFR1 and EGFR mediated signaling as well as downstream MAPKs. The expression of Sbi significantly contributed to IL-6 production and modulated CXCL-1 expression as well as neutrophil recruitment to the site of infection, thus demonstrating for the first time its relevance as a pro-inflammatory staphylococcal antigen in an in vivo model.

Indexed as

AnimalsBacterial ProteinsBinding Sites, AntibodyCarrier ProteinsChemokine CXCL1ErbB ReceptorsExtracellular Signal-Regulated MAP KinasesFemaleFlavonoidsImidazolesImmunoglobulin GInflammationInterleukin-6MiceMice, Inbred BALB CMice, Inbred C57BL2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazoleBacterial ProteinsCarrier ProteinsChemokine CXCL1Cxcl1 protein, mouseEGFR protein, mouseErbB ReceptorsExtracellular Signal-Regulated MAP KinasesFlavonoidsImidazolesImmunoglobulin GInterleukin-6p38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsPyridinesQuinazolinesReceptors, Tumor Necrosis Factor, Type IRTKI cpdSbi protein, Staphylococcus aureusStaphylococcal Protein ATyrphostinsVirulence Factors

Identifiers

PMID26126119
PMCPMC4488394
OpenAlexW782031982

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.