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@ARTICLE{OldeHeuvel:282965,
      author       = {Olde Heuvel, Florian and Zhang, Jin and Sun, Fan and
                      Krishnamurthy, Sruthi Sankari and Yartas, Gizem and Özkan,
                      Burak and Pagliarini, Marica and Voehringer, David and
                      O'Meara, Caitlin C and Schäfer, Michael K E and Huber-Lang,
                      Markus and Roselli, Francesco},
      title        = {{B}asophils activate splenic {B} cells and dendritic cells
                      via {IL}-13 signaling in acute traumatic brain injury.},
      journal      = {Journal of neuroinflammation},
      volume       = {22},
      number       = {1},
      issn         = {1742-2094},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {DZNE-2025-01417},
      pages        = {290},
      year         = {2025},
      abstract     = {Peripheral consequences following traumatic brain injury
                      (TBI) are characterized by both systemic inflammatory
                      responses and autonomic dysregulation. One of the main
                      immune regulatory organs, the spleen, shows high interaction
                      with the brain which is controlled by both circulating
                      mediators as well as autonomic fibers targeting splenic
                      immune cells. The brain-spleen axis does not function as a
                      one-way street, it also shows reciprocal effects where the
                      spleen affects neuroinflammatory and cognitive functions
                      post injury. To date, systemic and splenic inflammatory
                      responses are measured by cells or mediators located in
                      circulation. Nevertheless, most of the signaling and
                      inflammation post injury takes place in the organs.We set
                      out to investigate the early (3 h) signaling landscape in
                      the spleen following a moderate severity closed head injury
                      model to wild-type animals aged p60-90. Using
                      phospho-proteomic signaling approaches, immunofluorescence
                      stainings, Enzyme-Linked Immunosorbent Assay (ELISA),
                      super-resolution microscopy and single mRNA in situ
                      hybridization we investigated novel molecular and cellular
                      players in the spleen involved in immune modulation after a
                      head injury.Based on the signaling signature, we found a
                      rapid influx of basophil granulocytes towards the spleen,
                      via a recruitment mechanism that includes CXCL1 expressed by
                      B-cells and dendritic cells (DCs). The basophils in turn
                      seem to activate B cells and dendritic cells via the
                      IL-13/IL-13Ra1 signaling pathway and enhance protein
                      translation through the long non-coding RNA NORAD. The early
                      recruitment of basophils and subsequent activation of B
                      cells and DCs, is short lived and sets at 3dpi.
                      Interestingly, the rapid recruitment of basophils is
                      inhibited by ethanol intoxication in TBI, with a subsequent
                      prevention of IL-13Ra phosphorylation and NORAD increase in
                      B-cells and DCs.Basophils recruitment to the spleen may
                      serve as an early mediator of systemic inflammatory
                      responses to TBI with potential implications for research on
                      biomarkers and therapeutic targets.},
      keywords     = {Animals / Brain Injuries, Traumatic: immunology / Brain
                      Injuries, Traumatic: metabolism / Brain Injuries, Traumatic:
                      pathology / Mice / Spleen: immunology / Spleen: metabolism /
                      Spleen: pathology / Signal Transduction: physiology /
                      B-Lymphocytes: metabolism / B-Lymphocytes: immunology /
                      Interleukin-13: metabolism / Interleukin-13: immunology /
                      Basophils: metabolism / Basophils: immunology / Mice, Inbred
                      C57BL / Dendritic Cells: metabolism / Dendritic Cells:
                      immunology / Male / B-cell (Other) / Basophil (Other) /
                      Dendritic cell (Other) / IL-13 (Other) / Spleen (Other) /
                      Traumatic brain injury (Other) / Interleukin-13 (NLM
                      Chemicals)},
      cin          = {AG Roselli},
      ddc          = {610},
      cid          = {I:(DE-2719)1910001},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41408561},
      doi          = {10.1186/s12974-025-03621-1},
      url          = {https://pub.dzne.de/record/282965},
}