Journal Article

DZNE-2025-00870

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Transcriptomic profile of microglia following inflammation-sensitized hypoxic-ischemic brain injury in neonatal rats suggests strong contribution to neutrophil chemotaxis and activation.

Bremer, A.-S. (First author)DZNE* ; Henschel, N.DZNE* ; Burkard, H.DZNE* ; Bernis, M. E.DZNE* ; Ulas, T.DZNE* ; Sabir, H. (Last author)DZNE*

2025
BioMed Central London

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Please use a persistent id in citations: doi:10.1186/s12974-025-03516-1

Abstract: Inflammation-sensitized hypoxic-ischemic brain injury significantly contributes to neonatal mortality as affected neonates do not benefit from standard cooling treatments. To get further insight into inflammatory responses involved, we experimentally investigated the immune response of microglia in an inflammation-sensitized neonatal hypoxia-ischemia (HI) model.Transcriptomic analysis of microglia isolated from brains following inflammation-sensitized HI brain injury revealed a strong upregulation of leukocyte recruitment and pro-inflammatory markers. Specifically, markers associated with neutrophil-mediated immune responses and chemotaxis were upregulated in the inflammation-sensitized HI group compared to the non-inflammation-sensitized HI and control groups. Serpine 1 and Selp could be identified as specifically upregulated markers indicating an acute inflammatory condition before HI injury.Our study revealed preliminary data about a microglia population which is primed to recruit peripheral neutrophils to infiltrate the brain and mediate neutrophil immune response. We showed a contribution to neutrophil activation in case of inflammation following HI in the brain. Targeting microglia-mediated neutrophil recruitment can indicate a possible treatment approach in case of inflammation-sensitized HI brain injury.

Keyword(s): Animals (MeSH) ; Microglia: metabolism (MeSH) ; Microglia: pathology (MeSH) ; Hypoxia-Ischemia, Brain: pathology (MeSH) ; Hypoxia-Ischemia, Brain: metabolism (MeSH) ; Hypoxia-Ischemia, Brain: immunology (MeSH) ; Hypoxia-Ischemia, Brain: genetics (MeSH) ; Animals, Newborn (MeSH) ; Rats (MeSH) ; Neutrophils: metabolism (MeSH) ; Neutrophils: immunology (MeSH) ; Transcriptome: physiology (MeSH) ; Inflammation: pathology (MeSH) ; Inflammation: metabolism (MeSH) ; Neutrophil Activation: physiology (MeSH) ; Chemotaxis: physiology (MeSH) ; Gene Expression Profiling (MeSH) ; Rats, Sprague-Dawley (MeSH) ; Brain inflammation ; Microglia priming ; Neonatal Hypoxia-Ischemia ; Neutrophil recruitment ; Transcriptomic analysis

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Contributing Institute(s):

1. Neonatal Neuroscience (AG Sabir)
2. Molecular and Translational Immunaging (AG Bonaguro)
3. Clinical Single Cell Omics (CSCO) / Systems Medicine (AG Schultze)

Research Program(s):

1. 352 - Disease Mechanisms (POF4-352) (POF4-352)
2. 354 - Disease Prevention and Healthy Aging (POF4-354) (POF4-354)

Appears in the scientific report 2025

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