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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},
}