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@ARTICLE{Breer:276776,
      author       = {Breßer, Mona and Siemens, Kevin D and Schneider, Linda and
                      Lunnebach, Jonah E and Leven, Patrick and Glowka, Tim R and
                      Oberländer, Kristin and De Domenico, Elena and Schultze,
                      Joachim L and Schmidt, Joachim and Kalff, Jörg C and
                      Schneider, Anja and Wehner, Sven and Schneider, Reiner},
      title        = {{M}acrophage-induced enteric neurodegeneration leads to
                      motility impairment during gut inflammation.},
      journal      = {EMBO molecular medicine},
      volume       = {17},
      number       = {2},
      issn         = {1757-4676},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DZNE-2025-00315},
      pages        = {301 - 335},
      year         = {2025},
      abstract     = {Current studies pictured the enteric nervous system and
                      macrophages as modulators of neuroimmune processes in the
                      inflamed gut. Expanding this view, we investigated the
                      impact of enteric neuron-macrophage interactions on
                      postoperative trauma and subsequent motility disturbances,
                      i.e., postoperative ileus. In the early postsurgical phase,
                      we detected strong neuronal activation, followed by
                      transcriptional and translational signatures indicating
                      neuronal death and synaptic damage. Simultaneously, our
                      study revealed neurodegenerative profiles in
                      macrophage-specific transcriptomes after postoperative
                      trauma. Validating the role of resident and monocyte-derived
                      macrophages, we depleted macrophages by CSF-1R-antibodies
                      and used CCR2-/- mice, known for reduced monocyte
                      infiltration, in POI studies. Only CSF-1R-antibody-treated
                      animals showed decreased neuronal death and lessened
                      synaptic decay, emphasizing the significance of resident
                      macrophages. In human gut samples taken early and late
                      during abdominal surgery, we substantiated the mouse model
                      data and found reactive and apoptotic neurons and
                      dysregulation in synaptic genes, indicating a species'
                      overarching mechanism. Our study demonstrates that surgical
                      trauma activates enteric neurons and induces
                      neurodegeneration, mediated by resident macrophages,
                      introducing neuroprotection as an option for faster recovery
                      after surgery.},
      keywords     = {Animals / Macrophages: metabolism / Humans / Mice /
                      Gastrointestinal Motility / Enteric Nervous System:
                      pathology / Enteric Nervous System: physiopathology /
                      Disease Models, Animal / Inflammation: pathology / Neurons:
                      pathology / Neurons: metabolism / Mice, Inbred C57BL / Male
                      / Mice, Knockout / Enteric Neurons (Other) / Macrophages
                      (Other) / Neuroimmune Interaction (Other) / Postoperative
                      Ileus (Other) / Synaptic Damage (Other)},
      cin          = {AG Schneider / AG Schultze / PRECISE},
      ddc          = {610},
      cid          = {I:(DE-2719)1011305 / I:(DE-2719)1013038 /
                      I:(DE-2719)1013031},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 354 -
                      Disease Prevention and Healthy Aging (POF4-354) / 352 -
                      Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-354 /
                      G:(DE-HGF)POF4-352},
      experiment   = {EXP:(DE-2719)PRECISE-20190321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39762650},
      pmc          = {pmc:PMC11822118},
      doi          = {10.1038/s44321-024-00189-w},
      url          = {https://pub.dzne.de/record/276776},
}