ArticleInfection and immunity2009
Staphylococcus aureus induces microglial inflammation via a glycogen synthase kinase 3beta-regulated pathway.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 43 citations in OpenAlex.
- The influence of marine fungal meroterpenoid meroantarctine A toward HaCaT keratinocytes infected with Staphylococcus aureus.The Journal of antibiotics · 2024Article
- A Protective Role of Canonical Wnt/Mediators of inflammation · 2024Review
- Role of Glycogen Synthase Kinase-3 in Interferon-γ-Mediated Immune Hepatitis.International journal of molecular sciences · 2022Review
- Antimicrobial responses of peripheral and central nervous system glia against Staphylococcus aureus.Scientific reports · 2021Article
- The Potential Role of Inflammation in Modulating Endogenous Hippocampal Neurogenesis After Spinal Cord Injury.Frontiers in neuroscience · 2021Review
- Glycogen Synthase Kinase-3β Mediates Proinflammatory Cytokine Secretion and Adipogenesis in Orbital Fibroblasts from Patients with Graves' Orbitopathy.Investigative ophthalmology & visual science · 2020Article
- Review
- Pro-Inflammatory Stimuli Influence Expression of Intercellular Adhesion Molecule 1 in Human Anulus Fibrosus Cells through FAK/ERK/GSK3 and PKCδ Signaling Pathways.International journal of molecular sciences · 2018Article
- Dextromethorphan Attenuates NADPH Oxidase-Regulated Glycogen Synthase Kinase 3β and NF-κB Activation and Reduces Nitric Oxide Production in Group A Streptococcal Infection.Antimicrobial agents and chemotherapy · 2018Article
- The ubiquitin ligase ZNRF1 promotes caveolin-1 ubiquitination and degradation to modulate inflammation.Nature communications · 2017Article
- Cobalt Protoporphyrin Upregulates Cyclooxygenase-2 Expression Through a Heme Oxygenase-Independent Mechanism.Molecular neurobiology · 2016Article
- Glycogen synthase kinase 3β in Toll-like receptor signaling.BMB reports · 2016Review
- Lupus nephritis: glycogen synthase kinase 3β promotion of renal damage through activation of the NLRP3 inflammasome in lupus-prone mice.Arthritis & rheumatology (Hoboken, N.J.) · 2015Article
- Association of glycogen synthase kinase-3β with Parkinson's disease (review).Molecular medicine reports · 2014Review
- GSK3β and the control of infectious bacterial diseases.Trends in microbiology · 2014Review
- Glycogen synthase kinase-3 inhibitors: Rescuers of cognitive impairments.Pharmacology & therapeutics · 2014Review
- An emerging role for the anti-inflammatory cytokine interleukin-10 in dengue virus infection.Journal of biomedical science · 2013Review
- Contribution of toll-like receptor 2 to the innate response against Staphylococcus aureus infection in mice.PloS one · 2013Article
- Regulatory role of GSK-3 β on NF- κ B, nitric oxide, and TNF- α in group A streptococcal infection.Mediators of inflammation · 2013Article
- Role of glycogen synthase kinase-3 beta in the inflammatory response caused by bacterial pathogens.Journal of inflammation (London, England) · 2012Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A proinflammatory role for glycogen synthase kinase 3beta (GSK-3beta) has been demonstrated. Here, we addressed its roles on heat-inactivated Staphylococcus aureus-induced microglial inflammation. Heat-inactivated S. aureus induced tumor necrosis factor alpha (TNF-alpha) and nitric oxide (NO) production, at least in part, via a Toll-like receptor 2-regulated pathway. Neutralization of TNF-alpha largely blocked heat-inactivated S. aureus-induced NO. Heat-inactivated S. aureus activated GSK-3beta, and inhibiting GSK-3beta reduced TNF-alpha production as well as inducible NO synthase (iNOS)/NO biosynthesis. While activation of NF-kappaB was essential for heat-inactivated S. aureus-induced TNF-alpha and NO, inhibiting GSK-3beta blocked heat-inactivated S. aureus-induced NF-kappaB p65 nuclear translocation. Additionally, inhibiting GSK-3beta enhanced heat-inactivated S. aureus-induced interleukin-10 (IL-10) production (IL-10 is an anti-inflammatory cytokine which inhibits TNF-alpha production). Neutralization of IL-10 reduced TNF-alpha downregulation caused by GSK-3beta inhibition. These results suggest that GSK-3beta regulates heat-inactivated S. aureus-induced TNF-alpha and NO production in microglia mainly by activating NF-kappaB and probably by inhibiting IL-10.
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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.