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@ARTICLE{Rabenstein:873614,
      author       = {Rabenstein, Monika and Vay, Sabine Ulrike and Blaschke,
                      Stefan and Walter, Helene Luise and Ladwig, Anne and Fink,
                      Gereon Rudolf and Rueger, Maria Adele and Schroeter,
                      Michael},
      title        = {{C}rosstalk between stressed brain cells: direct and
                      indirect effects of ischemia and aglycemia on microglia},
      journal      = {Journal of neuroinflammation},
      volume       = {17},
      number       = {1},
      issn         = {1742-2094},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {FZJ-2020-00857},
      pages        = {33},
      year         = {2020},
      abstract     = {BackgroundIn cerebral ischemia, microglia have a
                      dichotomous role in keeping the balance between pro- and
                      anti-inflammatory mediators to avoid deleterious chronic
                      inflammation and to leverage repair processes.MethodsWe
                      examined functional and inflammatory markers in primary rat
                      microglia in vitro after oxygen-glucose deprivation (OGD) or
                      glucose deprivation (aglycemia). We then investigated the
                      preconditioning effect of OGD or aglycemia upon a subsequent
                      strong inflammatory stimulus, here lipopolysaccharides
                      (LPS). Moreover, an “in vitro brain model” of neurons
                      and glia, differentiated from primary rat neural stem cells,
                      was exposed to OGD or aglycemia. Conditioned medium (CM) of
                      this neuronal/glial co-culture was then used to condition
                      microglia, followed by LPS as a “second hit.”ResultsOGD
                      or aglycemia at sublethal doses did not significantly affect
                      microglia function, including the expression of inflammatory
                      markers. However, preconditioning with either OGD or
                      aglycemia led to a decreased pro-inflammatory response to a
                      subsequent stimulus with LPS. Interestingly, the
                      anti-inflammatory markers IGF-1 and IL-10 were additionally
                      reduced after such preconditioning, while expression of
                      CD206 remained unaffected. Treatment with CM from the
                      neuronal/glial co-culture alone did not affect the
                      expression of inflammatory markers in microglia. In
                      contrast, treatment with CM increased the expression of both
                      pro- and anti-inflammatory markers in microglia upon a
                      second hit with LPS. Interestingly, this effect could be
                      attenuated in microglia treated with CM from neuronal/glia
                      co-cultures preconditioned with OGD or
                      aglycemia.ConclusionsData suggest specific and distinct
                      microglia signatures in response to metabolic stress. While
                      metabolic stress directly and indirectly applied to
                      microglia did not mitigate their subsequent response to
                      inflammation, preconditioning with metabolic stress factors
                      such as OGD and aglycemia elicited a decreased inflammatory
                      response to a subsequent inflammation stimulus.},
      cin          = {INM-3},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406},
      pnm          = {572 - (Dys-)function and Plasticity (POF3-572)},
      pid          = {G:(DE-HGF)POF3-572},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31980036},
      UT           = {WOS:000513712000001},
      doi          = {10.1186/s12974-020-1697-8},
      url          = {https://juser.fz-juelich.de/record/873614},
}