Evidence map›Paper›PMID 34330996›Full record

ArticleCommunications biology2021

Acetate sensing by GPR43 alarms neutrophils and protects from severe sepsis.

Katja Schlatterer, Christian Beck, Ulrich Schoppmeier, Andreas Peschel, Dorothee Kretschmer

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 23 citations in OpenAlex.

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  11. Gut microbiota-mediated pain sensitization: mechanisms and therapeutic implications.Frontiers in pain research (Lausanne, Switzerland) · 2025
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  20. Short-Chain Fatty Acid and FFAR2 Activation - A New Option for Treating Infections?Frontiers in cellular and infection microbiology · 2021
    Review
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

5 authors at 1 institution in 1 country.

Katja SchlattererInterfaculty Institute for Microbiology and Infection Medicine Tübingen (IMIT), Infection Biology, University of Tübingen, Tübingen, Germany.
Christian BeckInterfaculty Institute for Microbiology and Infection Medicine Tübingen (IMIT), Infection Biology, University of Tübingen, Tübingen, Germany.
Ulrich SchoppmeierGerman Center for Infection Research, partner site Tübingen, Tübingen, Germany.
Andreas PeschelInterfaculty Institute for Microbiology and Infection Medicine Tübingen (IMIT), Infection Biology, University of Tübingen, Tübingen, Germany. andreas.peschel@uni-tuebingen.de.ORCID http://orcid.org/0000-0002-3209-8626
Dorothee KretschmerInterfaculty Institute for Microbiology and Infection Medicine Tübingen (IMIT), Infection Biology, University of Tübingen, Tübingen, Germany.
German Center for Infection Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bacterial sepsis is a major cause of mortality resulting from inadequate immune responses to systemic infection. Effective immunomodulatory approaches are urgently needed but it has remained elusive, which targets might be suitable for intervention. Increased expression of the G-protein-coupled receptor GPR43, which is known to govern intestinal responses to acetate, has been associated with sepsis patient survival but the mechanisms behind this observation have remained unclear. We show that elevated serum acetate concentrations prime neutrophils in a GPR43-dependent fashion, leading to enhanced neutrophil chemotaxis, oxidative burst, cytokine release and upregulation of phagocytic receptors. Consequently, acetate priming improved the capacity of human neutrophils to eliminate methicillin-resistant Staphylococcus aureus. Acetate administration increased mouse serum acetate concentrations and primed neutrophils. Notably, it rescued wild-type mice from severe S. aureus sepsis and reduced bacterial numbers in peripheral organs by several magnitudes. Acetate treatment improved the sepsis course even when applied several hours after onset of the infection, which recommends GPR43 as a potential target for sepsis therapy. Our study indicates that the severity of sepsis depends on transient neutrophil priming by appropriate blood acetate concentrations. Therapeutic interventions based on GPR43 stimulation could become valuable strategies for reducing sepsis-associated morbidity and mortality.

Indexed as

AcetatesMethicillin-Resistant Staphylococcus aureusNeutrophilsReceptors, G-Protein-CoupledSepsisStaphylococcal InfectionsAcetatesFfar2 protein, mouseReceptors, G-Protein-Coupled

Identifiers

PMID34330996
PMCPMC8324776
OpenAlexW3185424926

What OpenQuestion holds

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LicenceCC BY
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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.