% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Tuz:301568,
      author       = {A. A. Tuz and S. Ghosh and L. Karsch and M. Antler and V.
                      Lakovic and S. Lohmann and A. H. Lehmann and A. Beer and D.
                      Nagel and M. Jung and N. Hörenbaum and V. Kaygusuz and A.
                      Qefalia and B. Alshaar and N. Amookazemi and S. Bolsega and
                      M. Basic and J. T. Siveke$^*$ and S. Heiles and A.
                      Grüneboom and S. Lueong$^*$ and J. Herz and A. Sickmann and
                      N. Hagemann and A. Hasenberg and D. M. Hermann and M. Gunzer
                      and V. Singh},
      title        = {{G}ut microbiota deficiency reduces neutrophil activation
                      and is protective after ischemic stroke.},
      journal      = {Journal of neuroinflammation},
      volume       = {22},
      number       = {1},
      issn         = {1742-2094},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {DKFZ-2025-01076},
      pages        = {137},
      year         = {2025},
      abstract     = {Neutrophils are readily activated immune cells after
                      ischemic stroke in mice and patients. Still, the impact of
                      gut microbiota on neutrophil activation and its influence on
                      inflammatory brain injury remain undefined. We report that
                      natural microbiota colonization of germ-free (GF) mice
                      induces substantial neutrophil activation and deteriorates
                      stroke pathology. The colonized Ex-GF stroke mice had
                      considerably larger infarct sizes and higher sensorimotor
                      deficits than GF littermates. Furthermore, employing an
                      antibiotic-based mouse model of microbiota deficiency, we
                      demonstrate that gut microbiota depletion induces a juvenile
                      neutrophil phenotype characterized by the upregulation of
                      resting state surface receptors, reduced inflammatory
                      proteins, and levels of circulating NETs. This disarming of
                      neutrophil responses was associated with decreased
                      expression of brain inflammatory genes, vascular thrombus
                      formation, reduced infarct size, and alleviated behavioral
                      deficits. We conclude that gut microbes strongly influence
                      neutrophil activation after stroke and thus directly
                      contribute to stroke severity.},
      keywords     = {Animals / Gastrointestinal Microbiome: physiology /
                      Gastrointestinal Microbiome: immunology / Mice / Neutrophil
                      Activation: physiology / Ischemic Stroke: pathology /
                      Ischemic Stroke: immunology / Ischemic Stroke: microbiology
                      / Ischemic Stroke: prevention $\&$ control / Mice, Inbred
                      C57BL / Male / Neutrophils / Germ-Free Life / Gut microbiota
                      (Other) / Inflammation (Other) / Ischemic stroke (Other) /
                      Neutrophils (Other)},
      cin          = {ED01},
      ddc          = {610},
      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:40410847},
      pmc          = {pmc:PMC12100894},
      doi          = {10.1186/s12974-025-03448-w},
      url          = {https://inrepo02.dkfz.de/record/301568},
}