ArticleMediators of inflammation2013
Regulatory role of GSK-3 β on NF- κ B, nitric oxide, and TNF- α in group A streptococcal infection.
Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 37 citations in OpenAlex.
- Chicken Glycogen Synthase Kinase 3β Suppresses Innate Immune Responses and Enhances Avian Leukosis Virus Replication in DF-1 Cells.Microbiology spectrum · 2023Article
- Glycogen Synthase Kinase 3Stem cells international · 2022Article
- The Potential Role of Inflammation in Modulating Endogenous Hippocampal Neurogenesis After Spinal Cord Injury.Frontiers in neuroscience · 2021Review
- Involvement of 5-Hydroxytryptamine Receptor 2A in the Pathophysiology of Medication-Overuse Headache.Journal of pain research · 2021Article
- Review
- TLR7 Stimulation With Imiquimod Induces Selective Autophagy and ControlsFrontiers in microbiology · 2020Article
- Particles from the Echinococcus granulosus Laminated Layer Inhibit CD40 Upregulation in Dendritic Cells by Interfering with Akt Activation.Infection and immunity · 2019Article
- Streptolysin S induces mitochondrial damage and macrophage death through inhibiting degradation of glycogen synthase kinase-3β in Streptococcus pyogenes infection.Scientific reports · 2019Article
- Bacterial Manipulation of Wnt Signaling: A Host-Pathogen Tug-of-Wnt.Frontiers in immunology · 2019Review
- HECT E3 Ubiquitin Ligase-Regulated Txnip Degradation Facilitates TLR2-Mediated Inflammation During Group A Streptococcal Infection.Frontiers in immunology · 2019Article
- GSK3β inhibition attenuates LPS-induced IL-6 expression in porcine adipocytes.Scientific reports · 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
- Abscisic acid induces a transient shift in signaling that enhances NF-κB-mediated parasite killing in the midgut of Anopheles stephensi without reducing lifespan or fecundity.Parasites & vectors · 2017Article
- Effects of a GSK-3β inhibitor on the renal expression levels of RANK, RANKL and NF-κB in a rat model of diabetic nephropathy.Experimental and therapeutic medicine · 2016Article
- Protection against Klebsiella pneumoniae using lithium chloride in an intragastric infection model.Antimicrobial agents and chemotherapy · 2015Article
- Influenza A virus infection of vascular endothelial cells induces GSK-3β-mediated β-catenin degradation in adherens junctions, with a resultant increase in membrane permeability.Archives of virology · 2015Article
- GSK3β and the control of infectious bacterial diseases.Trends in microbiology · 2014Review
- GSK-3β inhibition attenuates CLP-induced liver injury by reducing inflammation and hepatic cell apoptosis.Mediators of inflammation · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Group A streptococcus (GAS) imposes a great burden on humans. Efforts to minimize the associated morbidity and mortality represent a critical issue. Glycogen synthase kinase-3 β (GSK-3 β) is known to regulate inflammatory response in infectious diseases. However, the regulation of GSK-3 β in GAS infection is still unknown. The present study investigates the interaction between GSK-3 β , NF- κ B, and possible related inflammatory mediators in vitro and in a mouse model. The results revealed that GAS could activate NF- κ B, followed by an increased expression of inducible nitric oxide synthase (iNOS) and NO production in a murine macrophage cell line. Activation of GSK-3 β occurred after GAS infection, and inhibition of GSK-3 β reduced iNOS expression and NO production. Furthermore, GSK-3 β inhibitors reduced NF- κ B activation and subsequent TNF- α production, which indicates that GSK-3 β acts upstream of NF- κ B in GAS-infected macrophages. Similar to the in vitro findings, administration of GSK-3 β inhibitor in an air pouch GAS infection mouse model significantly reduced the level of serum TNF- α and improved the survival rate. The inhibition of GSK-3 β to moderate the inflammatory effect might be an alternative therapeutic strategy against GAS infection.
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