Evidence map›Paper›PMID 28724977›Full record

ArticleScientific reports2017

Therapeutic targeting of HMGB1 during experimental sepsis modulates the inflammatory cytokine profile to one associated with improved clinical outcomes.

Natalie E Stevens, Marianne J Chapman, Cara K Fraser, Tim R Kuchel, John D Hayball, Kerrilyn R Diener

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
9.0field-weighted citation impact, top 1% 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Progress in the mechanistic understanding of NETs formation in cancer.Medical oncology (Northwood, London, England) · 2025
    Review
  6. Dysregulated neural coding in the vagus nerve during long sepsis.Brain, behavior, & immunity - health · 2025
    Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
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  19. Using heparan sulfate octadecasaccharide (18-mer) as a multi-target agent to protect against sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  20. Review

6 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

Natalie E StevensExperimental Therapeutics Laboratory, Hanson Institute, and Sansom Institute for Health Research, School of Pharmacy and Medical Science, University of South Australia, Adelaide, SA, Australia.
Marianne J ChapmanIntensive Care Unit, Royal Adelaide Hospital, Adelaide, SA, Australia.
Cara K FraserPreclinical, Imaging and Research Laboratories, South Australian Health and Medical Research Institute, Gilles Plains, Adelaide, SA, Australia.
Tim R KuchelPreclinical, Imaging and Research Laboratories, South Australian Health and Medical Research Institute, Gilles Plains, Adelaide, SA, Australia.
John D HayballExperimental Therapeutics Laboratory, Hanson Institute, and Sansom Institute for Health Research, School of Pharmacy and Medical Science, University of South Australia, Adelaide, SA, Australia. john.hayball@unisa.edu.au.
Kerrilyn R DienerExperimental Therapeutics Laboratory, Hanson Institute, and Sansom Institute for Health Research, School of Pharmacy and Medical Science, University of South Australia, Adelaide, SA, Australia. kerrilyn.diener@adelaide.edu.au.ORCID 0000-0001-8417-5542
University of South Australia · AUSouth Australian Health and Medical Research Institute · AURoyal Adelaide Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis remains a significant health burden and a major clinical need exists for therapeutics to dampen the excessive and uncontrolled immune activation. Nuclear protein high mobility group box protein 1 (HMGB1) is released following cell death and is a late mediator in sepsis pathogenesis. While approaches targeting HMGB1 have demonstrated reduced mortality in pre-clinical models of sepsis, the impact of HMGB1 blockade on the complex septic inflammatory milieu and the development of subsequent immunosuppression remain enigmatic. Analysis of plasma samples obtained from septic shock patients established an association between increased HMGB1 and non-survival, higher APACHE II scores, and increased pro-inflammatory cytokine responses. Pre-clinically, administration of neutralising ovine anti-HMGB1 polyclonal antibodies improved survival in murine endotoxaemia and caecal ligation and puncture-induced sepsis models, and altered early cytokine profiles to one which corresponded to patterns observed in the surviving patient cohort. Additionally, anti-HMGB1 treated murine sepsis survivors were significantly more resistant to secondary bacterial infection and exhibited altered innate immune cell phenotypes and cytokine responses. These findings demonstrate that anti-HMGB1 antibodies alter inflammation in murine sepsis models and reduce sepsis mortality without potentiating immunosuppression.

Indexed as

Molecular Targeted TherapyAgedAnimalsCecumCohort StudiesCytokinesDendritic CellsDisease Models, AnimalEndotoxemiaFemaleHMGB1 ProteinHumansInflammationLigationMacrophagesMaleCytokinesHMGB1 Protein

Identifiers

PMID28724977
PMCPMC5517568
OpenAlexW2734566932

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.