Chronic exposure to exogenous glucocorticoids primes microglia to pro-inflammatory stimuli and induces NLRP3 mRNA in the hippocampus

摘要: Chronic stress as well chronic treatment with glucocorticoids (GCs) primes the neuroinflammatory response to a subsequent pro-inflammatory challenge. However, it remains unclear whether GCs sensitize of key CNS immune substrates (i.e. microglia) stimuli. In present set studies, male Sprague-Dawley rats underwent sham surgery or were adrenalectomized and then treated varying concentrations corticosterone (CORT; 0, 25, 50, 75 μg/ml) administered in their drinking water. After 10 days CORT exposure, whole hippocampus was collected expression glial activation markers measured hippocampal microglia isolated challenged LPS probe for CORT-induced sensitization responses. exposure increased gene NLRP3, Iba-1, MHCII, NF-κBIα concentration dependent manner. (75 potentiated microglial proinflammatory (TNFα, IL-1β, IL-6 NLRP3) compared animals vehicle. The results demonstrate that stimuli add growing body evidence suggesting permissive function is an endogenous danger signal alarmin.