Home > Publications Database > Transcriptomic profile of microglia following inflammation-sensitized hypoxic-ischemic brain injury in neonatal rats suggests strong contribution to neutrophil chemotaxis and activation. > print

001     280026
005     20250824001719.0
024 7 _ |a 10.1186/s12974-025-03516-1
|2 doi
024 7 _ |a pmid:40684206
|2 pmid
024 7 _ |a altmetric:179512056
|2 altmetric
037 _ _ |a DZNE-2025-00870
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Bremer, Anna-Sophie
|0 P:(DE-2719)9001591
|b 0
|e First author
|u dzne
245 _ _ |a Transcriptomic profile of microglia following inflammation-sensitized hypoxic-ischemic brain injury in neonatal rats suggests strong contribution to neutrophil chemotaxis and activation.
260 _ _ |a London
|c 2025
|b BioMed Central
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1755684582_25772
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a 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.
536 _ _ |a 352 - Disease Mechanisms (POF4-352)
|0 G:(DE-HGF)POF4-352
|c POF4-352
|f POF IV
|x 0
536 _ _ |a 354 - Disease Prevention and Healthy Aging (POF4-354)
|0 G:(DE-HGF)POF4-354
|c POF4-354
|f POF IV
|x 1
588 _ _ |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
650 _ 7 |a Brain inflammation
|2 Other
650 _ 7 |a Microglia priming
|2 Other
650 _ 7 |a Neonatal Hypoxia-Ischemia
|2 Other
650 _ 7 |a Neutrophil recruitment
|2 Other
650 _ 7 |a Transcriptomic analysis
|2 Other
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Microglia: metabolism
|2 MeSH
650 _ 2 |a Microglia: pathology
|2 MeSH
650 _ 2 |a Hypoxia-Ischemia, Brain: pathology
|2 MeSH
650 _ 2 |a Hypoxia-Ischemia, Brain: metabolism
|2 MeSH
650 _ 2 |a Hypoxia-Ischemia, Brain: immunology
|2 MeSH
650 _ 2 |a Hypoxia-Ischemia, Brain: genetics
|2 MeSH
650 _ 2 |a Animals, Newborn
|2 MeSH
650 _ 2 |a Rats
|2 MeSH
650 _ 2 |a Neutrophils: metabolism
|2 MeSH
650 _ 2 |a Neutrophils: immunology
|2 MeSH
650 _ 2 |a Transcriptome: physiology
|2 MeSH
650 _ 2 |a Inflammation: pathology
|2 MeSH
650 _ 2 |a Inflammation: metabolism
|2 MeSH
650 _ 2 |a Neutrophil Activation: physiology
|2 MeSH
650 _ 2 |a Chemotaxis: physiology
|2 MeSH
650 _ 2 |a Gene Expression Profiling
|2 MeSH
650 _ 2 |a Rats, Sprague-Dawley
|2 MeSH
700 1 _ |a Henschel, Nico
|0 P:(DE-2719)9003171
|b 1
|u dzne
700 1 _ |a Burkard, Hannah
|0 P:(DE-2719)9002524
|b 2
|u dzne
700 1 _ |a Bernis, Maria Eugenia
|0 P:(DE-2719)2810557
|b 3
|u dzne
700 1 _ |a Ulas, Thomas
|0 P:(DE-2719)9000845
|b 4
|u dzne
700 1 _ |a Sabir, Hemmen
|0 P:(DE-2719)9000732
|b 5
|e Last author
|u dzne
773 _ _ |a 10.1186/s12974-025-03516-1
|g Vol. 22, no. 1, p. 189
|0 PERI:(DE-600)2156455-3
|n 1
|p 189
|t Journal of neuroinflammation
|v 22
|y 2025
|x 1742-2094
856 4 _ |u https://pub.dzne.de/record/280026/files/DZNE-2025-00870%20SUP.docx
856 4 _ |y OpenAccess
|u https://pub.dzne.de/record/280026/files/DZNE-2025-00870.pdf
856 4 _ |u https://pub.dzne.de/record/280026/files/DZNE-2025-00870%20SUP.doc
856 4 _ |u https://pub.dzne.de/record/280026/files/DZNE-2025-00870%20SUP.odt
856 4 _ |u https://pub.dzne.de/record/280026/files/DZNE-2025-00870%20SUP.pdf
856 4 _ |u https://pub.dzne.de/record/280026/files/DZNE-2025-00870.pdf?subformat=pdfa
|x pdfa
|y OpenAccess
909 C O |o oai:pub.dzne.de:280026
|p openaire
|p open_access
|p VDB
|p driver
|p dnbdelivery
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 0
|6 P:(DE-2719)9001591
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 1
|6 P:(DE-2719)9003171
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 2
|6 P:(DE-2719)9002524
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 3
|6 P:(DE-2719)2810557
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 4
|6 P:(DE-2719)9000845
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 5
|6 P:(DE-2719)9000732
913 1 _ |a DE-HGF
|b Gesundheit
|l Neurodegenerative Diseases
|1 G:(DE-HGF)POF4-350
|0 G:(DE-HGF)POF4-352
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Disease Mechanisms
|x 0
913 1 _ |a DE-HGF
|b Gesundheit
|l Neurodegenerative Diseases
|1 G:(DE-HGF)POF4-350
|0 G:(DE-HGF)POF4-354
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Disease Prevention and Healthy Aging
|x 1
914 1 _ |y 2025
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
|d 2024-12-16
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0160
|2 StatID
|b Essential Science Indicators
|d 2024-12-16
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
|d 2024-12-16
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1190
|2 StatID
|b Biological Abstracts
|d 2024-12-16
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0600
|2 StatID
|b Ebsco Academic Search
|d 2024-12-16
915 _ _ |a OpenAccess
|0 StatID:(DE-HGF)0510
|2 StatID
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b J NEUROINFLAMM : 2022
|d 2024-12-16
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0501
|2 StatID
|b DOAJ Seal
|d 2024-04-10T15:42:04Z
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0500
|2 StatID
|b DOAJ
|d 2024-04-10T15:42:04Z
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1030
|2 StatID
|b Current Contents - Life Sciences
|d 2024-12-16
915 _ _ |a Fees
|0 StatID:(DE-HGF)0700
|2 StatID
|d 2024-12-16
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
|d 2024-12-16
915 _ _ |a WoS
|0 StatID:(DE-HGF)0113
|2 StatID
|b Science Citation Index Expanded
|d 2024-12-16
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b ASC
|d 2024-12-16
915 _ _ |a Article Processing Charges
|0 StatID:(DE-HGF)0561
|2 StatID
|d 2024-12-16
915 _ _ |a IF >= 5
|0 StatID:(DE-HGF)9905
|2 StatID
|b J NEUROINFLAMM : 2022
|d 2024-12-16
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
|d 2024-12-16
915 _ _ |a Creative Commons Attribution CC BY 4.0
|0 LIC:(DE-HGF)CCBY4
|2 HGFVOC
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
|d 2024-12-16
920 1 _ |0 I:(DE-2719)5000032
|k AG Sabir
|l Neonatal Neuroscience
|x 0
920 1 _ |0 I:(DE-2719)1016005
|k AG Bonaguro
|l Molecular and Translational Immunaging
|x 1
920 1 _ |0 I:(DE-2719)1013038
|k AG Schultze
|l Clinical Single Cell Omics (CSCO) / Systems Medicine
|x 2
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a UNRESTRICTED
980 _ _ |a I:(DE-2719)5000032
980 _ _ |a I:(DE-2719)1016005
980 _ _ |a I:(DE-2719)1013038
980 1 _ |a FullTexts

LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21