Glucocorticoids mediate stress induction of the alarmin HMGB1 and reduction of the microglia checkpoint receptor CD200R1 in limbic brain structures.

ABSTRACT: Exposure to stressors primes neuroinflammatory responses to subsequent immune challenges and stress-induced glucocorticoids (GCs) play a mediating role in this phenomenon of neuroinflammatory priming. Recent evidence also suggests that the alarmin high-mobility group box-1 (HMGB1) and the microglial checkpoint receptor CD200R1 serve as proximal mechanisms of stress-induced neuroinflammatory priming. However, it is unclear whether stress-induced GCs play a causal role in these proximal mechanisms of neuroinflammatory priming; this forms the focus of the present investigation. Here, we found that exposure to a severe acute stressor (inescapable tailshock) induced HMGB1 and reduced CD200R1 expression in limbic brain regions and pharmacological blockade of GC signaling (RU486) mitigated these

SUBMITTER: Frank MG 

PROVIDER: S-EPMC6662571 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature