ArticleJournal of neuroinflammation2009
Lipopolysaccharide-induced interleukin-6 production is controlled by glycogen synthase kinase-3 and STAT3 in the brain.
Article in Journal of neuroinflammation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers.
What it found
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Who cites it
134 citing papers in PubMed, 235 citations in OpenAlex.
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- Calcium signaling in human and mouse microglia exhibit differential susceptibility to phytocannabinoids.Cell communication and signaling : CCS · 2026Article
- Interleukin-6, CD8Frontiers in aging neuroscience · 2026Review
- A Reporter Platform to Study Therapy-Induced Senescence in Live Cancer Cells.Small methods · 2025Article
- Biochemical, histopathological, and immunohistochemical study on the ameliorative effect of crocin against lipopolysaccharide‑induced hippocampal toxicity in male albino rats.BMC pharmacology & toxicology · 2025Article
- A Novel Iodine-Dextrin Complex Exhibits No Acute or Subacute Toxicity and Enhances Azithromycin Efficacy in an LPS-Induced Sepsis Model.Pharmaceutics · 2025Article
- Acute inflammation triggered by two lightweight hernia meshes: a comparative in vitro and retrospective cohort study.Hernia : the journal of hernias and abdominal wall surgery · 2025Article
- Fast Lithium-Releasing Phosphate Glasses Promote the Resolution of Inflammation.ACS applied bio materials · 2025Article
- Comparative Analysis of Bacteriome in Hair Follicle Layers of Patients with Female Pattern Androgenic Alopecia.Microorganisms · 2025Article
- Glycogen Synthase Kinase-3β Inhibitor VP3.15 Ameliorates Neurogenesis, Neuronal Loss and Cognitive Impairment in a Model of Germinal Matrix-intraventricular Hemorrhage of the Preterm Newborn.Translational stroke research · 2025Article
- Immunomodulatory Potential of Kaempferol Isolated fromInternational journal of molecular sciences · 2025Article
- Retrieval of conditioned immune response in male mice is mediated by an anterior-posterior insula circuit.Nature neuroscience · 2025Article
- Jing Guan Fang, an herbal formula, as an immunomodulator: opposing effects on basal and lipopolysaccharide-induced inflammation of macrophage via JAK/STAT3 and MAPK pathways.Frontiers in pharmacology · 2025Article
- Partial depletion of circulating neutrophil granulocytes in mice exacerbates the inflammatory response and hypothermia during LPS induced severe systemic inflammation.Frontiers in immunology · 2025Article
- Early responses of primary human and bovine monocytes, monocytic THP-1 cells and THP-1 cell-derived macrophages to vitalFrontiers in immunology · 2025Article
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- Microglia-induced neuroinflammation in hippocampal neurogenesis following traumatic brain injury.Heliyon · 2024Review
74 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundSeptic shock is a prevalent condition that, when not lethal, often causes disturbances in cognition, mood, and behavior, particularly due to central actions of the inflammatory cytokine interleukin-6 (IL-6). To identify potential targets to control brain IL-6, we tested if IL-6 produced by glia is regulated by signal transducer and activator of transcription-3 (STAT3) and glycogen synthase kinase-3 (GSK3).
methodsLipopolysaccharide (LPS) was used to induce inflammatory responses in mice or cultured primary glia. IL-6 was measured by ELISA and other inflammatory molecules were measured using an array.
resultsMouse brain IL-6 levels increased after central, as well as peripheral, LPS administration, consistent with glia producing a portion of brain IL-6. STAT3 in the brain was activated after peripheral or central LPS administration, and in LPS-stimulated cultured primary glia. Inhibition of STAT3 expression, function, or activation reduced by ~80% IL-6 production by primary glia, demonstrating the dependence on active STAT3. GSK3 promotes STAT3 activation, and array analysis of inflammatory molecules produced by LPS-stimulated primary glia demonstrated that IL-6 was the cytokine most diminished (>90%) by GSK3 inhibition. Inhibition of GSK3, and knockdown of GSK3beta, not GSK3alpha, greatly inhibited IL-6 production by LPS-stimulated primary glia. Conversely, expression of active STAT3 and active GSK3 promoted IL-6 production. In vivo inhibition of GSK3 reduced serum and brain IL-6 levels, brain STAT3 activation, and GFAP upregulation following LPS administration.
conclusionSTAT3 and GSK3 cooperatively promote neuroinflammation, providing novel targets for anti-inflammatory intervention.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.