Glucocorticoids exacerbate lipopolysaccharide-induced signaling in the frontal cortex and hippocampus in a dose-dependent manner

Munhoz, Carolina Demarchi; Sorrells, Shawn F.; Caso, Javier R.; Scavone, Cristoforo; Sapolsky, Robert M.

doi:10.1523/jneurosci.0303-09.2010

Cited by 169Neuroinflammation and Neurodegeneration MechanismsStress Responses and CortisolNF-κB Signaling Pathways

Glucocorticoids exacerbate lipopolysaccharide-induced signaling in the frontal cortex and hippocampus in a dose-dependent manner

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Munhoz, Carolina Demarchi, Sorrells, Shawn F., Caso, Javier R., Scavone, Cristoforo, Sapolsky, Robert M.·2010·The Journal of Neuroscience

DOI 10.1523/jneurosci.0303-09.2010PMC PMC3842494

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Abstract

Although the anti-inflammatory actions of glucocorticoids (GCs) are well established, evidence has accumulated showing that proinflammatory GC effects can occur in the brain, in a poorly understood manner. Using electrophoretic mobility shift assay, real-time PCR, and immunoblotting, we investigated the ability of varying concentrations of corticosterone (CORT, the GC of rats) to modulate lipopolysaccharide (LPS)-induced activation of NF-κB (nuclear factor κB), expression of anti- and proinflammatory factors and of the MAP (mitogen-activated protein) kinase family [ERK (extracellular signal-regulated kinase), p38, and JNK/SAPK (c-Jun N-terminal protein kinase/stress-activated protein kinase)], and AKT. In the frontal cortex, elevated CORT levels were proinflammatory, exacerbating LPS effects on NF-κB, MAP kinases, and proinflammatory gene expression. Milder proinflammatory GCs effects occurred in the hippocampus. In the absence of LPS, elevated CORT levels increased basal activation of ERK1/2, p38, SAPK/JNK, and AKT in both regions. These findings suggest that GCs do not uniformly suppress neuroinflammation and can even enhance it at multiple levels in the pathway linking LPS exposure to inflammation.

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Severe or mild deficiency in plasma corticosterone significantly enhanced NF-kappaB activation in the brain of rodents challenged with systemic LPS.
“More recently, Munhoz and colleagues demonstrated that a severe or mild deficiency in plasma corticosterone significantly enhanced NF-κB activation in the brain of rodents challenged with systemic LPS (134).”
From The HPA â€“ Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [134]

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Authors: Munhoz, C. D., Sorrells, S. F., Caso, J. R., Scavone, C., & Sapolsky, R. M.
Affiliations: Stanford University (US)
ORCID: Munhoz, Carolina Demarchi
Sorrells, Shawn F.
Caso, Javier R.
Sapolsky, Robert M.
Venue: The Journal of Neuroscience
Publisher: Society for Neuroscience
Published: 2010-10-13
Volume: 30
Issue: 41
Pages: 13690-13698
ISSN: 0270-6474 (ISSN-L)
1529-2401
DOI: 10.1523/jneurosci.0303-09.2010
PMC: PMC3842494
OpenAlex: W2058176183
Cited by: 169
References: 56
Citations by year: 2026: 4 · 2025: 7 · 2024: 11 · 2023: 7 · 2022: 6 · 2021: 11 · 2020: 12 · 2019: 14 · 2018: 14 · 2017: 11 · 2016: 9 · 2015: 10 · 2014: 10 · 2013: 16 · 2012: 14
FWCI: 8.13
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-sa
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 182 d)
Locations: Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Scientific Electronic Library Online (São Paulo Research Foundation, Latin American and Caribbean Center on Health Sciences Information, Conselho Nacional de Desenvolvimento Científico e Tecnológico) (publishedVersion)
Funders: Fundação de Amparo à Pesquisa do Estado de São Paulo (04/11041-0)
Conselho Nacional de Desenvolvimento Científico e Tecnológico
Ministerio de Ciencia e Innovación
National Institutes of Health (2r01mh053814-04, PO1 NS37520)
National Institute of Mental Health (R01 MH 53814)
National Institute of Neurological Disorders and Stroke (P01 NS 37520, P01NS037520)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords: glucocorticoids, corticosterone, lipopolysaccharide, neuroinflammation, NF-κB signaling, mitogen-activated protein kinase, ERK1/2, p38 MAPK, SAPK/JNK, Akt, frontal cortex, hippocampus, dose-dependent effects, pro-inflammatory gene expression
MeSH terms: Analysis of Variance, Animals, Corticosterone, Dose-Response Relationship, Drug, Frontal Lobe, Glucocorticoids, Hippocampus, Inflammation, Lipopolysaccharides, Male, Blotting, Western, Signal Transduction, NF-kappa B, Rats, Sprague-Dawley, Reverse Transcriptase Polymerase Chain Reaction, Electrophoretic Mobility Shift Assay, JNK Mitogen-Activated Protein Kinases, p38 Mitogen-Activated Protein Kinases, Proto-Oncogene Proteins c-akt, Rats

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Glucocorticoids exacerbate lipopolysaccharide-induced signaling in the frontal cortex and hippocampus in a dose-dependent manner

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