Evidence map›Paper›PMID 29455206›Full record

ArticleJournal of innate immunity2018

A Potential Mechanism for Immune Suppression by Beta-Adrenergic Receptor Stimulation following Traumatic Injury.

Nicholas J Shubin, Tam N Pham, Kristan Lea Staudenmayer, Brodie A Parent, Qian Qiu, Grant E O'Keefe

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

Article in Journal of innate immunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Observational
  3. Article
  4. Serious, Severe, Sepsis.Journal of innate immunity · 2020
    Article
  5. Who is WHO?Journal of innate immunity · 2020
    Article
  6. Tackling the Pros and Cons of Inflammation.Journal of innate immunity · 2019
    Article
  7. The Balancing Act of Inflammation.Journal of innate immunity · 2018
    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

6 authors at 3 institutions in 1 country.

Nicholas J ShubinSeattle Children's Research Institute, Seattle Children's Hospital, Seattle, Washington, USA.
Tam N PhamDepartment of Surgery, University of Washington, Seattle, Washington, USA.
Kristan Lea StaudenmayerDepartment of Surgery, Stanford University, Stanford, California, USA.
Brodie A ParentDepartment of Surgery, University of Washington, Seattle, Washington, USA.
Qian QiuHarborview Injury Prevention and Research Center, Department of Pediatrics, University of Washington, Seattle, Washington, USA.
Grant E O'KeefeHarborview Injury Prevention and Research Center, Department of Surgery, University of Washington, Seattle, Washington, USA.
University of Washington · USSeattle Children's Hospital · USStanford University · US

Funding

TRAUMA AND BURNST32GM007037 · NIGMS · UNIVERSITY OF WASHINGTON · PI O'KEEFE, GRANT E · 1985 to 2014
$3.3M
Surgery Research Training ProgramT32GM121290 · NIGMS · UNIVERSITY OF WASHINGTON · PI GRANT E O'KEEFE · 2017 to 2026
$2.8M
Gene Polymorphisms, Inflammation and Outcome from TraumaR01GM066946 · NIGMS · UNIVERSITY OF WASHINGTON · PI O'KEEFE, GRANT E · 2003 to 2007
$1.6M
NIGMS NIH HHS R01 GM066946NIGMS NIH HHS T32 GM007037NIGMS NIH HHS T32 GM121290
6 · The paper itself

Abstract

backgroundβ-Adrenergic agents suppress inflammation and may play an important role in posttraumatic infections. Mechanisms may include inhibition of MAP kinase signaling. We sought to determine whether MKP-1 contributed to catecholamine suppression of innate immunity and also wanted to know whether early catecholamine treatment after traumatic injury increases the risk of later nosocomial infection.

methodsWe performed experiments using THP-1 cells and peripheral blood mononuclear cells from healthy individuals. We exposed cells to epinephrine and/or LPS and measured inflammatory gene transcription and MAP kinase activation. We inhibited MKP-1 activity to determine its role in catecholamine-induced immune suppression. Finally, we studied injured subjects to determine whether early catecholamine treatment was associated with nosocomial infection.

resultsEpinephrine increases MKP-1 transcripts and protein and decreases LPS-induced p38 and JNK phosphorylation and TNF-α gene transcription. RNAi inhibition of MKP-1 at least partially restores LPS-induced TNF-α gene expression (p = 0.024). In the clinical cohort, subjects treated with β-adrenergic agents had an increased risk of ventilator-associated pneumonia (aOR = 1.9; 95% CI = 1.3-2.6) and bacteremia (aOR = 1.5; 95% CI = 1.1-2.3).

conclusionsMKP-1 may have a role in catecholamine-induced suppression of innate immunity, and exogenous catecholamines might contribute to nosocomial infection risk.

Indexed as

AdolescentAdrenergic beta-AgonistsAdultBacteremiaChildChild, PreschoolDual Specificity Phosphatase 1EpinephrineFemaleHumansImmunity, InnateInfantLeukocytes, MononuclearLipopolysaccharidesMaleMAP Kinase Signaling SystemAdrenergic beta-AgonistsDual Specificity Phosphatase 1DUSP1 protein, humanEpinephrineLipopolysaccharidesTumor Necrosis Factor-alphaVasoconstrictor AgentsHost defenseImmune responseKinasePhosphataseProteinSepsis

Identifiers

PMID29455206
PMCPMC6040823
OpenAlexW2794201635

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.