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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},
}