Evidence map›Paper›PMID 25766237›Full record

ArticleScience (New York, N.Y.)2015

Interleukin-3 amplifies acute inflammation and is a potential therapeutic target in sepsis.

Georg F Weber, Benjamin G Chousterman, Shun He, Ashley M Fenn, Manfred Nairz, Atsushi Anzai, Thorsten Brenner, Florian Uhle, Yoshiko Iwamoto, Clinton S Robbins and 13 more

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

Article in Science (New York, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 222 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
222citing papers in PubMed, 2 pooled it
22.0field-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

222 citing papers in PubMed, 2 syntheses or guidelines pooled it, 338 citations in OpenAlex.

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  16. Impaired peripheral mononuclear cell metabolism in patients at risk of developing sepsis: A cohort study.Journal of critical care medicine (Universitatea de Medicina si Farmacie din Targu-Mures) · 2026
    Article
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162 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors at 5 institutions in 2 countries.

Georg F WeberCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Department of Visceral, Thoracic and Vascular Surgery, Technische Universität Dresden, Dresden, Germany. fswirski@mgh.harvard.edu georg.weber@uniklinikum-dresden.de.
Benjamin G ChoustermanCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Shun HeCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Ashley M FennCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Manfred NairzCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Atsushi AnzaiCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Thorsten BrennerDepartment of Anesthesiology, University of Heidelberg, Heidelberg, Germany.
Florian UhleDepartment of Anesthesiology, University of Heidelberg, Heidelberg, Germany.
Yoshiko IwamotoCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Clinton S RobbinsCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Lorette NoiretCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Sarah L MaierDepartment of Visceral, Thoracic and Vascular Surgery, Technische Universität Dresden, Dresden, Germany.
Tina ZönnchenDepartment of Visceral, Thoracic and Vascular Surgery, Technische Universität Dresden, Dresden, Germany.
Nuh N RahbariDepartment of Visceral, Thoracic and Vascular Surgery, Technische Universität Dresden, Dresden, Germany.
Sebastian SchölchDepartment of Visceral, Thoracic and Vascular Surgery, Technische Universität Dresden, Dresden, Germany.
Anne Klotzsche-von AmelnDepartment of Clinical Pathobiochemistry and Institute for Clinical Chemistry and Laboratory Medicine, Technische Universität Dresden, Dresden, Germany.
Triantafyllos ChavakisDepartment of Clinical Pathobiochemistry and Institute for Clinical Chemistry and Laboratory Medicine, Technische Universität Dresden, Dresden, Germany.
Jürgen WeitzDepartment of Visceral, Thoracic and Vascular Surgery, Technische Universität Dresden, Dresden, Germany.
Stefan HoferDepartment of Anesthesiology, University of Heidelberg, Heidelberg, Germany.
Markus A WeigandDepartment of Anesthesiology, University of Heidelberg, Heidelberg, Germany.
Matthias NahrendorfCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Ralph WeisslederCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA.
Filip K SwirskiCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. fswirski@mgh.harvard.edu georg.weber@uniklinikum-dresden.de.
TU Dresden · DEMassachusetts General Hospital · USCenter for Systems Biology · USHeidelberg University · DEHarvard University · US

Funding

Monocyte Heterogeneity in Experimental and Human AtherosclerosisR01HL095612 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI SWIRSKI, FILIP K · 2009 to 2016
$3.4M
Innate Response Activator B cells in Bacterial Lung InfectionR56AI104695 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI SWIRSKI, FILIP K · 2013 to 2013
$403k
Austrian Science Fund FWF J 3486NHLBI NIH HHS 5R01HL095612NHLBI NIH HHS R01 HL095612NIAID NIH HHS R56 AI104695NIAID NIH HHS R56-AI104695
6 · The paper itself

Abstract

Sepsis is a frequently fatal condition characterized by an uncontrolled and harmful host reaction to microbial infection. Despite the prevalence and severity of sepsis, we lack a fundamental grasp of its pathophysiology. Here we report that the cytokine interleukin-3 (IL-3) potentiates inflammation in sepsis. Using a mouse model of abdominal sepsis, we showed that innate response activator B cells produce IL-3, which induces myelopoiesis of Ly-6C(high) monocytes and neutrophils and fuels a cytokine storm. IL-3 deficiency protects mice against sepsis. In humans with sepsis, high plasma IL-3 levels are associated with high mortality even after adjusting for prognostic indicators. This study deepens our understanding of immune activation, identifies IL-3 as an orchestrator of emergency myelopoiesis, and reveals a new therapeutic target for treating sepsis.

Indexed as

AnimalsB-Lymphocyte SubsetsCytokinesDisease Models, AnimalHumansInflammationInterleukin-3LipopolysaccharidesLymphoid TissueMiceMice, Inbred BALB CMonocytesMyelopoiesisNeutrophilsPeritonitisPrognosisCytokinesIL3 protein, humanInterleukin-3Lipopolysaccharides

Identifiers

PMID25766237
PMCPMC4376966
OpenAlexW2086143858

What OpenQuestion holds

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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.