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@ARTICLE{Richter:305622,
      author       = {M. Richter and E. Diesterbeck and E. Pylaeva$^*$ and N.
                      Labusek and C. Köster and D. Nagel and L. Karsch and A. J.
                      Fischer and M. Sous and M. Jung and R. Chevre and N.
                      Hagemann and E. A. Andersson and C. J. Ek and V. Singh and
                      D. M. Hermann and M. Gunzer and J. Jablonska$^*$ and U.
                      Felderhoff-Müser and I. Bendix and O. Soehnlein and J.
                      Herz},
      title        = {{H}ypoxic-ischemic brain injury in neonatal mice
                      sequentially recruits neutrophils with dichotomous phenotype
                      and function.},
      journal      = {Nature Communications},
      volume       = {16},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-02270},
      pages        = {9696},
      year         = {2025},
      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.},
      keywords     = {Animals / Hypoxia-Ischemia, Brain: immunology /
                      Hypoxia-Ischemia, Brain: pathology / Hypoxia-Ischemia,
                      Brain: physiopathology / Neutrophils: immunology /
                      Neutrophils: metabolism / Neutrophils: pathology / Animals,
                      Newborn / Phenotype / Mice / Neutrophil Infiltration / Mice,
                      Inbred C57BL / Brain: pathology / Brain: immunology /
                      Oligodendroglia: pathology / Male / Disease Models, Animal},
      cin          = {ED01},
      ddc          = {500},
      cid          = {I:(DE-He78)ED01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41184264},
      doi          = {10.1038/s41467-025-65517-1},
      url          = {https://inrepo02.dkfz.de/record/305622},
}