Corticosterone preexposure increases NF-κB translocation and sensitizes IL-1β responses in BV2 microglia-like cells

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dc.contributor.authorLiu, J.
dc.contributor.authorMustafa, S.
dc.contributor.authorBarratt, D.
dc.contributor.authorHutchinson, M.
dc.date.issued2018
dc.description.abstractCorticosterone (CORT), a critical mediator of the hypothalamus pituitary adrenal axis in rodents, is a stress hormone that is classically viewed as possessing immune-suppressive properties. CORT is now appreciated to also mediate the neuroimmune-priming effect of stress to innate-immune stimulation, and hence serves as a mechanistic link to the neuroimmune involvement in stress-related disorders. However, these dichotomous actions of CORT remain poorly defined. This study investigated the conditions and concentration dependency of CORT's actions required to prime the innate-immune system. Here, we measured the effect of CORT pretreatment on the downstream pro-inflammatory responses of BV2 mouse microglia-like cells stimulated by lipopolysaccharide (LPS). We quantified the concentration-dependent CORT-mediated attenuation and enhancement of LPS-stimulated inflammatory response. A high physiological concentration (500 nM) of CORT attenuated LPS-induced inflammatory IL-1β cytokine production in a glucocorticoid receptor-dependent manner. However, a low concentration (50 nM) of CORT increased expression and release of IL-1β in a mineralocorticoid receptor-dependent manner, with accompanied increases in NF-κB translocation and changes to related gene transcription. These results suggest that a mild elevation in CORT may cause selective adaptations in microglia-like cells to overrespond to a second immune challenge in a non-classical manner, thus partially explaining both pro- and anti-inflammatory effects of CORT reported in the literature.
dc.description.statementofresponsibilityJiaJun Liu, Sanam Mustafa, Daniel Thomas Barratt and Mark Rowland Hutchinson
dc.identifier.citationFrontiers in Immunology, 2018; 9(JAN):1-12
dc.identifier.doi10.3389/fimmu.2018.00003
dc.identifier.issn1664-3224
dc.identifier.issn1664-3224
dc.identifier.orcidLiu, J. [0000-0003-1887-0218]
dc.identifier.orcidMustafa, S. [0000-0002-8677-5151]
dc.identifier.orcidBarratt, D. [0000-0001-6261-353X]
dc.identifier.orcidHutchinson, M. [0000-0003-2154-5950]
dc.identifier.urihttp://hdl.handle.net/2440/111529
dc.language.isoen
dc.publisherFrontiers Media SA
dc.relation.granthttp://purl.org/au-research/grants/arc/CE140100003
dc.rightsCopyright © 2018 Liu, Mustafa, Barratt and Hutchinson. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
dc.source.urihttps://doi.org/10.3389/fimmu.2018.00003
dc.subjectCytokines; nF-κB, cell morphology; BV2 microglia cells; neuroendocrinology; glucocorticoids; glucocorticoid receptors; IL-1β
dc.titleCorticosterone preexposure increases NF-κB translocation and sensitizes IL-1β responses in BV2 microglia-like cells
dc.title.alternativeCorticosterone preexposure increases NF-kappaB translocation and sensitizes IL-1beta responses in BV2 microglia-like cells
dc.typeJournal article
pubs.publication-statusPublished

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