Evidence map›Paper›PMID 29691444›Full record

ArticleScientific reports2018

Adaptive response of neonatal sepsis-derived Group B Streptococcus to bilirubin.

Richard Hansen, Sophie Gibson, Eduardo De Paiva Alves, Mark Goddard, Andrew MacLaren, Anne Marie Karcher, Susan Berry, Elaina S R Collie-Duguid, Emad El-Omar, Mike Munro and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
4.4field-weighted citation impact, top 6% 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

10 citing papers in PubMed, 27 citations in OpenAlex.

  1. Bilirubin: translational perspectives.Pediatric research · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Observational
  7. Novel Compound HeterozygousFrontiers in cardiovascular medicine · 2022
    Article
  8. Article
  9. Article
  10. The role of microbiota in neonatal hyperbilirubinemia.American journal of translational research · 2020
    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

11 authors at 4 institutions in 2 countries.

Richard HansenDepartment of Paediatric Gastroenterology, Royal Hospital for Children, Glasgow, G51 4TF, United Kingdom. richard.hansen@nhs.net.ORCID 0000-0002-3944-6646
Sophie GibsonGastrointestinal Research Group, School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, United Kingdom.
Eduardo De Paiva AlvesCentre for Genome Enabled Biology and Medicine, University of Aberdeen, 23 St Machar Drive, Aberdeen, AB24 3RY, United Kingdom.
Mark GoddardGastrointestinal Research Group, School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, United Kingdom.
Andrew MacLarenNeonatal Unit, Aberdeen Maternity Hospital, Foresterhill, Aberdeen, AB25 2ZL, United Kingdom.
Anne Marie KarcherDepartment of Medical Microbiology, Aberdeen Royal Infirmary, Foresterhill, Aberdeen, AB25 2ZD, United Kingdom.
Susan BerryGastrointestinal Research Group, School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, United Kingdom.
Elaina S R Collie-DuguidCentre for Genome Enabled Biology and Medicine, University of Aberdeen, 23 St Machar Drive, Aberdeen, AB24 3RY, United Kingdom.ORCID 0000-0002-7511-4139
Emad El-OmarSt George and Sutherland Clinical School, University of New South Wales, Sydney, Australia.
Mike MunroNeonatal Unit, Aberdeen Maternity Hospital, Foresterhill, Aberdeen, AB25 2ZL, United Kingdom.
Georgina L HoldGastrointestinal Research Group, School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, United Kingdom. georgina.hold@unsw.edu.au.ORCID 0000-0001-7573-3397
University of Aberdeen · GBAberdeen Maternity Hospital · GBAberdeen Royal Infirmary · GBSutherland Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperbilirubinemia is so common in newborns as to be termed physiological. The most common bacteria involved in early-onset neonatal sepsis are Streptococcus agalactiae, commonly called Group B Streptococcus (GBS). Whilst previous studies show bilirubin has antioxidant properties and is beneficial in endotoxic shock, little thought has been given to whether bilirubin might have antibacterial properties. In this study, we performed a transcriptomic and proteomic assessment of GBS cultured in the presence/absence of bilirubin. Our analysis revealed that increasing levels of bilirubin (>100 µmol/L) negatively correlated with GBS growth (18% reduction from 0-400 µmol/L on plate model, p < 0.001; 33% reduction from 0-100 µmol/L in liquid model, p = 0.02). Transcriptome analysis demonstrated 19 differentially expressed genes, almost exclusively up-regulated in the presence of bilirubin. Proteomic analysis identified 12 differentially expressed proteins, half over-expressed in the presence of bilirubin. Functional analysis using Gene Ontology and KEGG pathways

Indexed as

BilirubinHumansHyperbilirubinemia, NeonatalInfant, NewbornJaundiceNeonatal SepsisProteomicsSepsisStreptococcal InfectionsStreptococcus agalactiaeTranscriptomeBilirubin

Identifiers

PMID29691444
PMCPMC5915570
OpenAlexW2801902068

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.