Evidence map›Paper›PMID 20577143›Full record

ArticleShock (Augusta, Ga.)2011

Systemic inflammation and liver injury following hemorrhagic shock and peripheral tissue trauma involve functional TLR9 signaling on bone marrow-derived cells and parenchymal cells.

Roop Gill, Xiangcai Ruan, Christoph L Menzel, Seung Namkoong, Patricia Loughran, David J Hackam, Timothy R Billiar

Abstract read
In one paragraph

Article in Shock (Augusta, Ga.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

27 citing papers in PubMed, 39 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Macrophages play an essential role in trauma-induced sterile inflammation and tissue repair.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2018
    Review
  8. Observational
  9. Mouse Injury Model of Polytrauma and Shock.Methods in molecular biology (Clifton, N.J.) · 2018
    Review
  10. Characterization of hypoalbuminemia following temporary abdominal closure.The journal of trauma and acute care surgery · 2017
    Article
  11. NK1.1Journal of leukocyte biology · 2017
    Article
  12. Time for trauma immunology.PLoS medicine · 2017
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Platelet-derived HMGB1 is a critical mediator of thrombosis.The Journal of clinical investigation · 2015
    Article
  18. Article
  19. Article
  20. Article
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 2 countries.

Roop GillDepartment of Surgery, University of Pittsburgh, 200 Lothrop St., Pittsburgh, PA 15213, USA. billiartr@upmc.edu
Xiangcai Ruan
Christoph L Menzel
Seung Namkoong
Patricia Loughran
David J Hackam
Timothy R Billiar
University of Pittsburgh · USGuangzhou First People's Hospital · CN

Funding

University of Pittsburgh Clinical and Translational Science InstituteUL1TR000005 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2012 to 2015
$50.8M
Regulation of Intestinal Mucosal Injury & Repair After Trauma/Hemorrhagic ShockP50GM053789 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI VODOVOTZ, YORAM · 1997 to 2013
$18.0M
TLR4 Signaling in the Pathogenesis of Surgical Necrotizing EnterocolitisR01GM078238 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HACKAM, DAVID J · 2006 to 2019
$3.9M
Modulation of TLR4 and TLR9 Signaling in NECR01DK083752 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HACKAM, DAVID J · 2008 to 2016
$3.4M
NCATS NIH HHS UL1 TR000005NIDDK NIH HHS R01 DK083752NIGMS NIH HHS GM-53789-09NIGMS NIH HHS P50 GM053789NIGMS NIH HHS R01 GM078238
6 · The paper itself

Abstract

Hemorrhagic shock due to trauma (HS/T) induces an inflammatory response that can contribute to end-organ injury. The pathways involved in the initiation and propagation of HS/T-induced inflammation are incompletely understood. Here, we hypothesized that the DNA sensor TLR9 would have a role in inflammatory signaling after HS/T. Using mice expressing a nonfunctional, mutant form of TLR9, we identified a role of TLR9 in driving the initial cytokine response and liver damage in a model of hemorrhagic shock and bilateral femur fracture. Circulating DNA levels were found to correlate with the degree of tissue damage. Experiments using chimeric mice show that TLR9 on both bone marrow-derived cells and parenchymal cells are important for the TLR9-mediated liver and tissue damage, as well as systemic inflammation after HS/T. These data suggest that release of DNA may be a driver of the inflammatory response to severe injury as well as a marker of the extent of tissue damage. One of the sensors of DNA in the setting of HS/T seems to be TLR9.

Indexed as

Signal TransductionAnimalsBone Marrow CellsInflammationLiverMiceMice, Mutant StrainsShock, HemorrhagicToll-Like Receptor 9Wounds and InjuriesTlr9 protein, mouseToll-Like Receptor 9

Identifiers

PMID20577143
PMCPMC3000874
OpenAlexW1986586703

What OpenQuestion holds

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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.