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@ARTICLE{Zhang:163745,
      author       = {Zhang, Jin and Li, Zhenghui and Chandrasekar, Akila and Li,
                      Shun and Ludolph, Albert and Böckers, Tobias and
                      Huber-Lang, Markus and Roselli, Francesco and Olde Heuvel,
                      Florian},
      title        = {{F}ast {M}aturation of {S}plenic {D}endritic {C}ells {U}pon
                      {TBI} {I}s {A}ssociated {W}ith {FLT}3/{FLT}3{L}
                      {S}ignaling.},
      journal      = {Frontiers in immunology},
      volume       = {13},
      issn         = {1664-3224},
      address      = {Lausanne},
      publisher    = {Frontiers Media},
      reportid     = {DZNE-2022-00484},
      pages        = {824459},
      year         = {2022},
      abstract     = {The consequences of systemic inflammation are a significant
                      burden after traumatic brain injury (TBI), with almost all
                      organs affected. This response consists of inflammation and
                      concurrent immunosuppression after injury. One of the main
                      immune regulatory organs, the spleen, is highly interactive
                      with the brain. Along this brain-spleen axis, both nerve
                      fibers as well as brain-derived circulating mediators have
                      been shown to interact directly with splenic immune cells.
                      One of the most significant comorbidities in TBI is acute
                      ethanol intoxication (EI), with almost $40\%$ of patients
                      showing a positive blood alcohol level (BAL) upon injury. EI
                      by itself has been shown to reduce proinflammatory mediators
                      dose-dependently and enhance anti-inflammatory mediators in
                      the spleen. However, how the splenic immune modulatory
                      effect reacts to EI in TBI remains unclear. Therefore, we
                      investigated early splenic immune responses after TBI with
                      and without EI, using gene expression screening of cytokines
                      and chemokines and fluorescence staining of thin spleen
                      sections to investigate cellular mechanisms in immune cells.
                      We found a strong FLT3/FLT3L induction 3 h after TBI, which
                      was enhanced by EI. The FLT3L induction resulted in
                      phosphorylation of FLT3 in CD11c+ dendritic cells, which
                      enhanced protein synthesis, maturation process, and the
                      immunity of dendritic cells, shown by pS6, peIF2A, MHC-II,
                      LAMP1, and CD68 by immunostaining and TNF-α expression by
                      in-situ hybridization. In conclusion, these data indicate
                      that TBI induces a fast maturation and immunity of dendritic
                      cells which is associated with FLT3/FLT3L signaling and
                      which is enhanced by EI prior to TBI.},
      keywords     = {Brain Injuries, Traumatic: metabolism / Dendritic Cells /
                      Humans / Inflammation / Membrane Proteins: genetics / Spleen
                      / fms-Like Tyrosine Kinase 3 / FLT3 (Other) / dendritic cell
                      (Other) / ethanol (Other) / spleen (Other) / traumatic brain
                      injury (Other)},
      cin          = {Clinical Study Center Ulm / AG Böckers / AG Roselli},
      ddc          = {610},
      cid          = {I:(DE-2719)5000077 / I:(DE-2719)1910002 /
                      I:(DE-2719)1910001},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 352 -
                      Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35281004},
      pmc          = {pmc:PMC8907149},
      doi          = {10.3389/fimmu.2022.824459},
      url          = {https://pub.dzne.de/record/163745},
}