Evidence map›Paper›PMID 35945238›Full record

ArticleNature communications2022

Microbe capture by splenic macrophages triggers sepsis via T cell-death-dependent neutrophil lifespan shortening.

Marianna Ioannou, Dennis Hoving, Iker Valle Aramburu, Mia I Temkin, Nathalia M De Vasconcelos, Theodora-Dorita Tsourouktsoglou, Qian Wang, Stefan Boeing, Robert Goldstone, Spyros Vernardis and 6 more

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

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

35 citing papers in PubMed, 65 citations in OpenAlex.

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  5. IL-15/NKG2D signaling-mediated activation of CD8Journal of thoracic disease · 2026
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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

16 authors at 4 institutions in 3 countries.

Marianna Ioannou *The Francis Crick Institute, Antimicrobial Defence Laboratory, London, UK.
Dennis Hoving *The Francis Crick Institute, Antimicrobial Defence Laboratory, London, UK.
Iker Valle AramburuThe Francis Crick Institute, Antimicrobial Defence Laboratory, London, UK.
Mia I TemkinThe Francis Crick Institute, Antimicrobial Defence Laboratory, London, UK.
Nathalia M De VasconcelosThe Francis Crick Institute, Antimicrobial Defence Laboratory, London, UK.
Theodora-Dorita TsourouktsoglouThe Francis Crick Institute, Antimicrobial Defence Laboratory, London, UK.
Qian WangThe Francis Crick Institute, Antimicrobial Defence Laboratory, London, UK.
Stefan BoeingThe Francis Crick Institute, Bioinformatics and Biostatistics, London, UK.
Robert GoldstoneThe Francis Crick Institute, Advanced Sequencing, London, UK.
Spyros VernardisThe Francis Crick Institute, Molecular Biology of Metabolism Laboratory, London, UK.ORCID 0000-0002-3946-1686
Vadim DemichevThe Francis Crick Institute, Molecular Biology of Metabolism Laboratory, London, UK.
Markus RalserThe Francis Crick Institute, Molecular Biology of Metabolism Laboratory, London, UK.
Sascha DavidInstitute for Intensive Care Medicine, University Hospital Zurich, Zurich, Switzerland.
Klaus StahlDepartment of Gastroenterology, Hepatology and Endocrinology, Medical School Hannover, Hannover, Germany.
Christian BodeDepartment of Anaesthesiology and Critical Care, University Hospital Bonn, Bonn, Germany.ORCID 0000-0002-0830-870X
Venizelos PapayannopoulosThe Francis Crick Institute, Antimicrobial Defence Laboratory, London, UK. veni.p@crick.ac.uk.ORCID 0000-0002-3741-8190
The Francis Crick Institute · GBMedizinische Hochschule Hannover · DEUniversity Hospital Bonn · DEUniversity Hospital of Zurich · CH

Funding

Cancer Research UK FC0010129Cancer Research UK FC001134Medical Research Council FC0010129Medical Research Council FC001134Wellcome Trust 222825/Z/21/ZWellcome Trust FC0010129Wellcome Trust FC001134
6 · The paper itself

Abstract

The mechanisms linking systemic infection to hyperinflammation and immune dysfunction in sepsis are poorly understood. Extracellular histones promote sepsis pathology, but their source and mechanism of action remain unclear. Here, we show that by controlling fungi and bacteria captured by splenic macrophages, neutrophil-derived myeloperoxidase attenuates sepsis by suppressing histone release. In systemic candidiasis, microbial capture via the phagocytic receptor SIGNR1 neutralizes myeloperoxidase by facilitating marginal zone infiltration and T cell death-dependent histone release. Histones and hyphae induce cytokines in adjacent CD169 macrophages including G-CSF that selectively depletes mature Ly6G

Indexed as

NeutrophilsSepsisGranulocyte Colony-Stimulating FactorHistonesHumansLongevityMacrophagesPeroxidaseT-LymphocytesGranulocyte Colony-Stimulating FactorHistonesPeroxidase

Identifiers

PMID35945238
PMCPMC9361272
OpenAlexW4291019402

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.