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000873614 1001_ $$0P:(DE-HGF)0$$aRabenstein, Monika$$b0
000873614 245__ $$aCrosstalk between stressed brain cells: direct and indirect effects of ischemia and aglycemia on microglia
000873614 260__ $$aLondon$$bBioMed Central$$c2020
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000873614 520__ $$aBackgroundIn 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.
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000873614 7001_ $$0P:(DE-HGF)0$$aVay, Sabine Ulrike$$b1
000873614 7001_ $$0P:(DE-HGF)0$$aBlaschke, Stefan$$b2
000873614 7001_ $$0P:(DE-HGF)0$$aWalter, Helene Luise$$b3
000873614 7001_ $$0P:(DE-HGF)0$$aLadwig, Anne$$b4
000873614 7001_ $$0P:(DE-Juel1)131720$$aFink, Gereon Rudolf$$b5$$ufzj
000873614 7001_ $$0P:(DE-HGF)0$$aRueger, Maria Adele$$b6
000873614 7001_ $$00000-0001-8441-4793$$aSchroeter, Michael$$b7$$eCorresponding author
000873614 773__ $$0PERI:(DE-600)2156455-3$$a10.1186/s12974-020-1697-8$$gVol. 17, no. 1, p. 33$$n1$$p33$$tJournal of neuroinflammation$$v17$$x1742-2094$$y2020
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