Modulation of inflammatory cytokines and mitogen-activated protein kinases by acetate in primary astrocytes

Soliman, Mahmoud L.; Combs, Colin K.; Rosenberger, Thad A.

doi:10.1007/s11481-012-9426-4

Cited by 84Neuroinflammation and Neurodegeneration MechanismsTryptophan and brain disordersNF-κB Signaling Pathways

Modulation of inflammatory cytokines and mitogen-activated protein kinases by acetate in primary astrocytes

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Soliman, Mahmoud L., Combs, Colin K., Rosenberger, Thad A.·2013·Journal of Neuroimmune Pharmacology

DOI 10.1007/s11481-012-9426-4PMC PMC3587660

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Abstract

Acetate supplementation attenuates neuroglia activation in a rat model of neuroinflammation by a mechanism associated with an increase in brain acetyl-CoA, an alteration in histone acetylation, and reduction of interleukin (IL)-1β expression. We propose that reduced astroglial activation occurs by disrupting astrocyte-derived inflammatory signaling and cytokine release. Using primary astroglial cultures, we found that LPS (0-25 ng/ml, 4 h) increased tumor necrosis factor (TNF-α) and IL-1β in a concentration-dependent manner, which was reduced by treatment with sodium acetate (12 mM). LPS did not alter H3K9 acetylation or IL-6 levels, whereas acetate treatment increased H3K9 acetylation by 2-fold and decreased basal levels of IL-6 by 2-fold. Acetate treatment attenuated the LPS-induced increase in TNF-α mRNA, but did not reverse the mRNA levels of other pro-inflammatory cytokines. By contrast, LPS decreased TGF-β1 and IL-4 protein and TGF-β1 mRNA, all of which was reversed with acetate treatment. Further, we found that acetate treatment completely reversed LPS-induced phosphorylation of MAPK p38 and decreased basal levels of phosphorylated extracellular signal-regulated kinases1/2 (ERK1/2) by 2-fold. Acetate treatment also reversed LPS-elevated NF-κB p65, CCAAT/enhancer-binding protein beta protein levels, and reduced basal levels of phosphorylated NF-κB p65 at serine 536. These results suggest that acetate treatment has a net anti-inflammatory effect in LPS-stimulated astrocytes that is largely associated with a disruption in MAPK and NF-κB signaling.

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Acetate modulates inflammatory cytokines and signaling pathways in astrocyte primary culture.
“acetate was also able to modulate inflammatory cytokines and signaling pathways in astrocyte primary culture (112).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [112]

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Ledeboer A Breve JJ Poole S Tilders FJ Van Dam AM 2000 Interleukin-10, interleukin-4, and transforming growth factor-beta differentially regulate lipopolysaccharide-induced production of pro-inflammatory cytokines and nitric oxide in co-cultures of rat astroglial and microglial cells Glia 30 134 142 10719355

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Neuroglial mechanisms involved in the anti-inflammatory effect of acetate supplementation
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Authors: Soliman, M. L., Combs, C. K., & Rosenberger, T. A.
Affiliations: University of North Dakota (US)
Corresponding author: Rosenberger, Thad A.
ORCID: Combs, Colin K.
Rosenberger, Thad A.
Venue: Journal of Neuroimmune Pharmacology
Publisher: Springer Science and Business Media LLC
Published: 2012-12-12
Volume: 8
Issue: 1
Pages: 287-300
ISSN: 1557-1890 (ISSN-L)
1557-1904
DOI: 10.1007/s11481-012-9426-4
PMC: PMC3587660
OpenAlex: W2053022788
Cited by: 84
References: 88
Citations by year: 2026: 3 · 2025: 14 · 2024: 8 · 2023: 1 · 2022: 13 · 2021: 11 · 2020: 5 · 2019: 2 · 2018: 1 · 2017: 7 · 2016: 5 · 2015: 4 · 2014: 2 · 2013: 8
FWCI: 2.26
Type: journal article
Language: en
Open access: green
europepmc.org
Licence: www.springer.com/tdm (tdm)
Locations: Journal of Neuroimmune Pharmacology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Center for Research Resources (P20RR017699)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords: acetate, sodium acetate, astrocytes, neuroinflammation, lipopolysaccharide, inflammatory cytokines, TNF-α, IL-1β, interleukin-6, TGF-β1, histone acetylation, H3K9 acetylation, acetyl-CoA, MAPK signaling, p38 MAPK, ERK1/2, NF-κB p65, C/EBPβ, anti-inflammatory activity
MeSH terms: Acetates, Acetyl Coenzyme A, Acetylation, Animals, Astrocytes, Cells, Cultured, Histones, Inflammation, L-Lactate Dehydrogenase, Lipopolysaccharides, Mice, Inbred C57BL, RNA, Messenger, Blotting, Western, Signal Transduction, Cytokines, NF-kappa B, In Situ Nick-End Labeling, Mitogen-Activated Protein Kinases, MAP Kinase Signaling System, CCAAT-Enhancer-Binding Proteins, Mice, Real-Time Polymerase Chain Reaction

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Modulation of inflammatory cytokines and mitogen-activated protein kinases by acetate in primary astrocytes

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