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Dexamethasone exhibits its anti-inflammatory effects in S. aureus induced microglial inflammation via modulating TLR-2 and glucocorticoid receptor expression
Published in Elsevier B.V.
PMID: 31401378
Volume: 75
Microglial inflammation plays crucial role in the pathogenesis of CNS infections including brain abscesses. Staphylococcus aureus (S. aureus) is considered as one of the major causative agents of brain abscesses. Due to the emergence of multidrug resistant bacteria the available treatment options including conventional antibiotics and steroid therapy become ineffective in terms of inflammation regulation which warrants further investigation to resolve this health issue. Microglial TLR-2 plays important roles in the bacterial recognition as well as induction of inflammation whereas glucocorticoid receptor (GR) triggers anti-inflammatory pathways in presence of glucocorticoids (GCs). The main objective of this study was to figure out the interdependency between TLR-2 and GR in presence of exogenous dexamethasone during microglial inflammation as an alternative therapeutic approach. Experiments were done either in TLR-2 neutralized condition or GR blocked condition in presence of dexamethasone. Free radicals production, arginase, superoxide dismutase (SOD), catalase enzyme activities and corticosterone concentration were measured along with Western blot analysis of TLR-2, GR and other inflammatory molecules. The results suggested that dexamethasone pre-treatment in TLR-2 neutralized condition efficiently reduces the inflammatory consequences of S. aureus induced microglial inflammation through up regulating GR expression. During TLR-2 blocking dexamethasone exerted its potent anti-inflammatory activities via suppressing reactive oxygen species (ROS), NO production and up regulating arginase, SOD and catalase activities at the time point of 90 min. Further in-vivo experiments are needed to conclude that dexamethasone could resolve brain inflammation possibly through microglial phenotypic switching from pro-inflammatory M1 to anti-inflammatory M2. © 2019
About the journal
JournalData powered by TypesetInternational Immunopharmacology
PublisherData powered by TypesetElsevier B.V.
Open AccessNo