Evidence map›Paper›PMID 23774593›Full record

ArticleInfection and immunity2013

Group B Streptococcus and Streptococcus suis capsular polysaccharides induce chemokine production by dendritic cells via Toll-like receptor 2- and MyD88-dependent and -independent pathways.

Cynthia Calzas, Guillaume Goyette-Desjardins, Paul Lemire, Fleur Gagnon, Claude Lachance, Marie-Rose Van Calsteren, Mariela Segura

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  9. Protein kinase D mediates inflammatory responses of human placental macrophages to Group B Streptococcus.American journal of reproductive immunology (New York, N.Y. : 1989) · 2019
    Article
  10. Article
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  12. Frontiers in microbiology · 2018
    Article
  13. Frontiers in immunology · 2018
    Article
  14. Article
  15. Article
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  17. Immune-responsiveness of CD4Scientific reports · 2016
    Article
  18. Article
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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

7 authors at 2 institutions in 1 country.

Cynthia CalzasLaboratory of Immunology, Faculty of Veterinary Medicine, University of Montreal, Saint-Hyacinthe, Quebec, Canada.
Guillaume Goyette-Desjardins
Paul Lemire
Fleur Gagnon
Claude Lachance
Marie-Rose Van Calsteren
Mariela Segura
Université de Montréal · CAAgriculture and Agri-Food Canada · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Streptococcus agalactiae (also known as group B Streptococcus [GBS]) and Streptococcus suis are encapsulated streptococci causing severe septicemia and meningitis. Bacterial capsular polysaccharides (CPSs) are poorly immunogenic, but anti-CPS antibodies are essential to the host defense against encapsulated bacteria. The mechanisms underlying anti-CPS antibody responses are not fully elucidated, but the biochemistry of CPSs, particularly the presence of sialic acid, may have an immunosuppressive effect. We investigated the ability of highly purified S. suis and GBS native (sialylated) CPSs to activate dendritic cells (DCs), which are crucial actors in the initiation of humoral immunity. The influence of CPS biochemistry was studied using CPSs extracted from different serotypes within these two streptococcal species, as well as desialylated CPSs. No interleukin-1β (IL-1β), IL-6, IL-12p70, tumor necrosis factor alpha (TNF-α), or IL-10 production was observed in S. suis or GBS CPS-stimulated DCs. Moreover, these CPSs exerted immunosuppressive effects on DC activation, as a diminution of gamma interferon (IFN-γ)-induced B cell-activating factor of the tumor necrosis factor family (BAFF) expression was observed in CPS-pretreated cells. However, S. suis and GBS CPSs induced significant production of CCL3, via partially Toll-like receptor 2 (TLR2)- and myeloid differentiation factor 88 (MyD88)-dependent pathways, and CCL2, via TLR-independent mechanisms. No major influence of CPS biochemistry was observed on the capacity to induce chemokine production by DCs, indicating that DCs respond to these CPSs in a patterned way rather than a structure-dedicated manner.

Indexed as

AnimalsB-Cell Activating FactorB-LymphocytesChemokine CCL3Dendritic CellsImmunity, HumoralInterferon-gammaInterleukinsLymphocyte ActivationMiceMice, Inbred C57BLMyeloid Differentiation Factor 88Polysaccharides, BacterialSignal TransductionStreptococcal InfectionsStreptococcus agalactiaeB-Cell Activating FactorCcl3 protein, mouseChemokine CCL3Interferon-gammaInterleukinsMyd88 protein, mouseMyeloid Differentiation Factor 88Polysaccharides, BacterialTlr2 protein, mouseTnfsf13b protein, mouseToll-Like Receptor 2Tumor Necrosis Factor-alpha

Identifiers

PMID23774593
PMCPMC3754219
OpenAlexW2034479706

What OpenQuestion holds

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Registered trials

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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.