Evidence map›Paper›PMID 26651945›Full record

ArticleCell host & microbe2015

Group B Streptococcus Evades Host Immunity by Degrading Hyaluronan.

Stacey L Kolar, Pierre Kyme, Ching Wen Tseng, Antoine Soliman, Amber Kaplan, Jiurong Liang, Victor Nizet, Dianhua Jiang, Ramachandran Murali, Moshe Arditi and 2 more

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

Article in Cell host & microbe, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

58 citing papers in PubMed, 105 citations in OpenAlex.

  1. Review
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  16. Biology · 2024
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  18. Function and contribution of two putativeInfection and immunity · 2024
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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

12 authors at 2 institutions in 1 country.

Stacey L KolarDivision of Pediatric Infectious Diseases, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Research Division of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Pierre KymeDivision of Pediatric Infectious Diseases, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Research Division of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Ching Wen TsengDivision of Pediatric Infectious Diseases, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Research Division of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Antoine SolimanDivision of Pediatric Infectious Diseases, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Research Division of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Amber KaplanResearch Division of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Jiurong LiangDivision of Pulmonary, Department of Medicine, and Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Victor NizetDepartment of Pediatrics and Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California San Diego, La Jolla, CA 92093, USA.
Dianhua JiangResearch Division of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Division of Pulmonary, Department of Medicine, and Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Ramachandran MuraliResearch Division of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Moshe ArditiDivision of Pediatric Infectious Diseases, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Research Division of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
David M UnderhillResearch Division of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
George Y LiuDivision of Pediatric Infectious Diseases, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Research Division of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA. Electronic address: george.liu@cshs.org.
Cedars-Sinai Medical Center · USUniversity of California San Diego · US

Funding

Glycoprotein Remodeling in the Vasculopathy and Coagulopathy of SepsisR01HL125352 · NHLBI · UNIVERSITY OF CALIFORNIA SANTA BARBARA · PI MARTH, JAMEY, NIZET, VICTOR · 2014 to 2018
$3.6M
The Cedars-Sinai Immunobiology Training ProgramT32AI089553 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI ARDITI, MOSHE, TARGAN, STEPHAN R. · 2010 to 2016
$1.1M
Bacterial Manipulation of Host Hyaluronan Degradation for Immune EvasionR21AI103839 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI LIU, GEORGE Y · 2013 to 2014
$447k
NHLBI NIH HHS R01 HL125352NIAID NIH HHS AI 10383-9NIAID NIH HHS R21 AI103839NIAID NIH HHS T32 AI089553NIAID NIH HHS T32 AI 89553-3Wellcome Trust
6 · The paper itself

Abstract

In response to tissue injury, hyaluronan (HA) polymers are cleaved by host hyaluronidases, generating small fragments that ligate Toll-like receptors (TLRs) to elicit inflammatory responses. Pathogenic bacteria such as group B Streptococcus (GBS) express and secrete hyaluronidases as a mechanism for tissue invasion, but it is not known how this activity relates to immune detection of HA. We found that bacterial hyaluronidases secreted by GBS and other Gram-positive pathogens degrade pro-inflammatory HA fragments to their component disaccharides. In addition, HA disaccharides block TLR2/4 signaling elicited by both host-derived HA fragments and other TLR2/4 ligands, including lipopolysaccharide. Application of GBS hyaluronidase or HA disaccharides reduced pulmonary pathology and pro-inflammatory cytokine levels in an acute lung injury model. We conclude that breakdown of host-generated pro-inflammatory HA fragments to disaccharides allows bacterial pathogens to evade immune detection and could be exploited as a strategy to treat inflammatory diseases.

Indexed as

Immune EvasionDisaccharidesHyaluronic AcidHyaluronoglucosaminidaseHydrolysisStreptococcus agalactiaeDisaccharidesHyaluronic AcidHyaluronoglucosaminidase

Identifiers

PMID26651945
PMCPMC4683412
OpenAlexW2196134238

What OpenQuestion holds

Textmetadata
LicenceTDM
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.