Evidence map›Paper›PMID 24890566›Full record

ArticleCritical care (London, England)2014

The role of CXCL10 in the pathogenesis of experimental septic shock.

Daniela S Herzig, Liming Luan, Julia K Bohannon, Tracy E Toliver-Kinsky, Yin Guo, Edward R Sherwood

Open access · goldAbstract read
In one paragraph

Article in Critical care (London, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

31 citing papers in PubMed, 48 citations in OpenAlex.

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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 2 countries.

Daniela S Herzig
Liming Luan
Julia K Bohannon
Tracy E Toliver-Kinsky
Yin Guo
Edward R Sherwood
Vanderbilt University Medical Center · USLudwig-Maximilians-Universität München · DEThe University of Texas Medical Branch at Galveston · US

Funding

Molecular Mechanisms of Environmental InjuryT32ES007254 · NIEHS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI AMEREDES, BILL T · 1990 to 2022
$6.6M
Resistance of Beta 2 Microglobulin Null Mice to SepsisR01GM066885 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI SHERWOOD, EDWARD R · 2003 to 2016
$4.4M
Augmentation of Innate Anti-Microbial Immunity by TLR4 AgonistsR01GM104306 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ENKHBAATAR, PERENLEI, SHERWOOD, EDWARD R · 2013 to 2016
$1.2M
NIEHS NIH HHS T32 ES007254NIGMS NIH HHS R01 GM066885NIGMS NIH HHS R01 GM104306NIGMS NIH HHS R01 GM66885
6 · The paper itself

Abstract

introductionThe chemokine CXCL10 is produced during infection and inflammation to activate the chemokine receptor CXCR3, an important regulator of lymphocyte trafficking and activation. The goal of this study was to assess the contributions of CXCL10 to the pathogenesis of experimental septic shock in mice.

methodsSeptic shock was induced by cecal ligation and puncture (CLP) in mice resuscitated with lactated Ringer's solution and, in some cases, the broad spectrum antibiotic Primaxin. Studies were performed in CXCL10 knockout mice and mice treated with anti-CXCL10 immunoglobulin G (IgG). Endpoints included leukocyte trafficking and activation, core body temperature, plasma cytokine concentrations, bacterial clearance and survival.

resultsCXCL10 was present at high concentrations in plasma and peritoneal cavity during CLP-induced septic shock. Survival was significantly improved in CXCL10 knockout (CXCL10KO) mice and mice treated with anti-CXCL10 IgG compared to controls. CXCL10KO mice and mice treated with anti-CXCL10 IgG showed attenuated hypothermia, lower concentrations of interleukin-6 (IL-6) and macrophage inhibitory protein-2 (MIP-2) in plasma and lessened natural killer (NK) cell activation compared to control mice. Compared to control mice, bacterial burden in blood and lungs was lower in CXCL10-deficient mice but not in mice treated with anti-CXCL10 IgG. Treatment of mice with anti-CXCL10 IgG plus fluids and Primaxin at 2 or 6 hours after CLP significantly improved survival compared to mice treated with non-specific IgG under the same conditions.

conclusionsCXCL10 plays a role in the pathogenesis of CLP-induced septic shock and could serve as a therapeutic target during the acute phase of septic shock.

Indexed as

AnimalsBody TemperatureChemokine CXCL10CytokinesFemaleImmunoglobulin GKiller Cells, NaturalLymphocyte ActivationMaleMice, Inbred C57BLMice, KnockoutPeritoneal CavityShock, SepticChemokine CXCL10CytokinesImmunoglobulin G

Identifiers

PMID24890566
PMCPMC4075230
OpenAlexW1987012257

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.