Evidence map›Paper›PMID 41184264›Full record

ArticleNature communications2025

Hypoxic-ischemic brain injury in neonatal mice sequentially recruits neutrophils with dichotomous phenotype and function.

Mathis Richter, Eva Diesterbeck, Ekaterina Pylaeva, Nicole Labusek, Christian Köster, Dennis Nagel, Laura Karsch, Alexa Josephine Fischer, Marah Sous, Marcel Jung and 12 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Article
  2. Review
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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

22 authors.

Mathis Richter *Department of Pediatrics I, Neonatology & Experimental Perinatal Neurosciences, University Hospital Essen, University Duisburg-Essen, Essen, Germany.ORCID http://orcid.org/0000-0002-3110-6137
Eva Diesterbeck *Department of Pediatrics I, Neonatology & Experimental Perinatal Neurosciences, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Ekaterina PylaevaDepartment of Otorhinolaryngology, Translational Oncology, University Hospital Essen, University Duisburg-Essen, Essen, Germany.ORCID http://orcid.org/0000-0002-3941-9664
Nicole LabusekDepartment of Pediatrics I, Neonatology & Experimental Perinatal Neurosciences, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Christian KösterDepartment of Pediatrics I, Neonatology & Experimental Perinatal Neurosciences, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Dennis NagelInstitute for Experimental Immunology and Imaging, University Hospital Essen, University Duisburg-Essen, Essen, Germany.ORCID http://orcid.org/0009-0004-2911-9301
Laura KarschInstitute for Experimental Immunology and Imaging, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Alexa Josephine FischerDepartment of Pediatrics I, Neonatology & Experimental Perinatal Neurosciences, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Marah SousDepartment of Pediatrics I, Neonatology & Experimental Perinatal Neurosciences, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Marcel JungInstitute for Experimental Immunology and Imaging, University Hospital Essen, University Duisburg-Essen, Essen, Germany.ORCID http://orcid.org/0000-0002-8277-3052
Raphael ChevreInstitute of Experimental Pathology (ExPat), Center of Molecular Biology of Inflammation (ZMBE), University of Münster, Münster, Germany.
Nina HagemannCenter for Translational Neuro- and Behavioral Sciences (C-TNBS), University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Erik Axel AnderssonDepartment of Molecular and Clinical Medicine, Institute of Medicine, Wallenberg Centre for Molecular and Translational Medicine, University of Gothenburg, Gothenburg, Sweden.
C Joakim EkInstitute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Vikramjeet SinghInstitute for Experimental Immunology and Imaging, University Hospital Essen, University Duisburg-Essen, Essen, Germany.ORCID http://orcid.org/0000-0002-7361-8317
Dirk M HermannCenter for Translational Neuro- and Behavioral Sciences (C-TNBS), University Hospital Essen, University Duisburg-Essen, Essen, Germany.ORCID http://orcid.org/0000-0003-0198-3152
Matthias GunzerInstitute for Experimental Immunology and Imaging, University Hospital Essen, University Duisburg-Essen, Essen, Germany.ORCID http://orcid.org/0000-0002-5534-6055
Jadwiga JablonskaDepartment of Otorhinolaryngology, Translational Oncology, University Hospital Essen, University Duisburg-Essen, Essen, Germany.ORCID http://orcid.org/0000-0003-1490-2542
Ursula Felderhoff-MüserDepartment of Pediatrics I, Neonatology & Experimental Perinatal Neurosciences, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Ivo BendixDepartment of Pediatrics I, Neonatology & Experimental Perinatal Neurosciences, University Hospital Essen, University Duisburg-Essen, Essen, Germany.ORCID http://orcid.org/0000-0002-9751-3640
Oliver SoehnleinInstitute of Experimental Pathology (ExPat), Center of Molecular Biology of Inflammation (ZMBE), University of Münster, Münster, Germany.ORCID http://orcid.org/0000-0002-7854-0694
Josephine HerzDepartment of Pediatrics I, Neonatology & Experimental Perinatal Neurosciences, University Hospital Essen, University Duisburg-Essen, Essen, Germany. josephine.herz@uk-essen.de.

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) HE- 7363/2-1
6 · The paper itself

Abstract

Neonatal encephalopathy caused by hypoxia-ischemia (HI) leads to a strong neutrophil infiltration. The long-held assumption that neutrophils act exclusively as tissue-damaging cells, is challenged by increasing evidence of a profound neutrophil heterogeneity. Here, we uncovered a pronounced phenotypical and functional diversification of neutrophils in neonatal mice depending on the disease stage. Neutrophil infiltration was biphasic, peaking 1 and 7 days after HI. Early brain-infiltrating neutrophils displayed a hyperactivated phenotype, whereas neutrophils at day 7 exhibited an angiogenic phenotype with high Siglec-F expression. Acute neutrophil depletion protected against neural cell death, associated with decreased hyperactivity in adolescent animals. Delayed neutrophil depletion impaired vascular and oligodendrocyte regeneration, resulting in exacerbated alterations of anxiety-related behavior and myelination deficits. These findings suggest a divergent function of neutrophils, with early neutrophils aggravating tissue damage and late neutrophils contributing to neurological recovery. The disease stage-dependent neutrophil diversification offers new possibilities to identify disease-stage-specific therapeutic targets.

Indexed as

Hypoxia-Ischemia, BrainNeutrophilsAnimalsBrainFemaleMaleMiceMice, Inbred C57BLNeurodegenerative DiseasesNeutrophil InfiltrationOligodendrogliaRegenerationVascular Remodeling

Identifiers

PMID41184264
PMCPMC12583616

What Socratic holds

Textmetadata
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 Socratic graph.