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@ARTICLE{Bremer:280026,
author = {Bremer, Anna-Sophie and Henschel, Nico and Burkard, Hannah
and Bernis, Maria Eugenia and Ulas, Thomas and Sabir,
Hemmen},
title = {{T}ranscriptomic profile of microglia following
inflammation-sensitized hypoxic-ischemic brain injury in
neonatal rats suggests strong contribution to neutrophil
chemotaxis and activation.},
journal = {Journal of neuroinflammation},
volume = {22},
number = {1},
issn = {1742-2094},
address = {London},
publisher = {BioMed Central},
reportid = {DZNE-2025-00870},
pages = {189},
year = {2025},
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.},
keywords = {Animals / Microglia: metabolism / Microglia: pathology /
Hypoxia-Ischemia, Brain: pathology / Hypoxia-Ischemia,
Brain: metabolism / Hypoxia-Ischemia, Brain: immunology /
Hypoxia-Ischemia, Brain: genetics / Animals, Newborn / Rats
/ Neutrophils: metabolism / Neutrophils: immunology /
Transcriptome: physiology / Inflammation: pathology /
Inflammation: metabolism / Neutrophil Activation: physiology
/ Chemotaxis: physiology / Gene Expression Profiling / Rats,
Sprague-Dawley / Brain inflammation (Other) / Microglia
priming (Other) / Neonatal Hypoxia-Ischemia (Other) /
Neutrophil recruitment (Other) / Transcriptomic analysis
(Other)},
cin = {AG Sabir / AG Bonaguro / AG Schultze},
ddc = {610},
cid = {I:(DE-2719)5000032 / I:(DE-2719)1016005 /
I:(DE-2719)1013038},
pnm = {352 - Disease Mechanisms (POF4-352) / 354 - Disease
Prevention and Healthy Aging (POF4-354)},
pid = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-354},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:40684206},
doi = {10.1186/s12974-025-03516-1},
url = {https://pub.dzne.de/record/280026},
}