Evidence map›Paper›PMID 23704792›Full record

ArticleMicrobiology (Reading, England)2013

The two-component response regulator LiaR regulates cell wall stress responses, pili expression and virulence in group B Streptococcus.

David C Klinzing, Nadeeza Ishmael, Julie C Dunning Hotopp, Hervé Tettelin, Kelly R Shields, Lawrence C Madoff, Karen M Puopolo

Open access · greenAbstract read
In one paragraph

Article in Microbiology (Reading, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
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  6. Article
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  8. Article
  9. Review
  10. Review
  11. Identification of DraRS inJournal of bacteriology · 2023
    Article
  12. Article
  13. Review
  14. Mechanisms of group BReproduction & fertility · 2022
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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 5 institutions in 1 country.

David C KlinzingHarvard Medical School, 25 Shattuck Street, Boston, MA 02115, USA.
Nadeeza IshmaelInstitute for Genome Sciences, University of Maryland Baltimore, 801 West Baltimore Street, Baltimore, MD 21201, USA.
Julie C Dunning HotoppInstitute for Genome Sciences, University of Maryland Baltimore, 801 West Baltimore Street, Baltimore, MD 21201, USA.
Hervé TettelinInstitute for Genome Sciences, University of Maryland Baltimore, 801 West Baltimore Street, Baltimore, MD 21201, USA.
Kelly R ShieldsChanning Laboratory, Brigham and Women's Hospital, 181 Longwood Avenue, Boston, MA 02115, USA.
Lawrence C MadoffMassachusetts Department of Public Health, Jamaica Plain, MA 02130, USA.
Karen M PuopoloHarvard Medical School, 25 Shattuck Street, Boston, MA 02115, USA.
Brigham and Women's Hospital · USJ. Craig Venter Institute · USLemuel Shattuck Hospital · USMassachusetts Department of Public Health · USUniversity of Maryland, Baltimore · US

Funding

Training Program in Newborn and Developmental DiseasesT32HD007466 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI KOUREMBANAS, STELLA · 1994 to 2016
$8.0M
GROUP B STREPTOCOCCAL SURFACE PROTEINS IN IMMUNE EVASIONR01AI038424 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI MADOFF, LAWRENCE C. · 1997 to 2005
$1.5M
Mechanisms of Tandem Repeat Deletion in Group B StrepK08HD041534 · NICHD · BRIGHAM AND WOMEN'S HOSPITAL · PI PUOPOLO, KAREN M · 2002 to 2006
$668k
NIAID NIH HHS R01 AI038424NIAID NIH HHS R01-AI38424NICHD NIH HHS HD041534NICHD NIH HHS K08 HD041534NICHD NIH HHS T32 HD007466NICHD NIH HHS T32-HD007466-11A1
6 · The paper itself

Abstract

Group B Streptococcus (GBS) remains the leading cause of early onset sepsis among term infants. Evasion of innate immune defences is critical to neonatal GBS disease pathogenesis. Effectors of innate immunity, as well as numerous antibiotics, frequently target the peptidoglycan layer of the Gram-positive bacterial cell wall. The intramembrane-sensing histidine kinase (IM-HK) class of two-component regulatory systems has been identified as important to the Gram-positive response to cell wall stress. We have characterized the GBS homologue of LiaR, the response regulator component of the Lia system, to determine its role in GBS pathogenesis. LiaR is expressed as part of a three-gene operon (liaFSR) with a promoter located upstream of liaF. A LiaR deletion mutant is more susceptible to cell wall-active antibiotics (vancomycin and bacitracin) as well as antimicrobial peptides (polymixin B, colistin, and nisin) compared to isogenic wild-type GBS. LiaR mutant GBS are significantly attenuated in mouse models of both GBS sepsis and pneumonia. Transcriptional profiling with DNA microarray and Northern blot demonstrated that LiaR regulates expression of genes involved in microbial defence against host antimicrobial systems including genes functioning in cell wall synthesis, pili formation and cell membrane modification. We conclude that the LiaFSR system, the first member of the IM-HK regulatory systems to be studied in GBS, is involved in sensing perturbations in the integrity of the cell wall and activates a transcriptional response that is important to the pathogenesis of GBS infection.

Indexed as

Gene Expression Regulation, BacterialSignal TransductionAnimalsAnti-Bacterial AgentsBacterial ProteinsCell WallDisease Models, AnimalFemaleFimbriae, BacterialHeat-Shock ResponseHumansInfant, NewbornMiceMolecular Sequence DataPneumonia, BacterialSepsisAnti-Bacterial AgentsBacterial Proteins

Identifiers

PMID23704792
PMCPMC3749725
OpenAlexW2010098507

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.