ArticleMolecular neurobiology2019
The Mycobacterial Adjuvant Analogue TDB Attenuates Neuroinflammation via Mincle-Independent PLC-γ1/PKC/ERK Signaling and Microglial Polarization.
Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- ERK1/2 activation in anti-inflammatory effects and underlying signaling mechanisms.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Targeting CLEC4E in immunosuppressive tumour-associated macrophages via BET inhibition.Clinical and translational medicine · 2025Article
- Berberine Exerts Neuroprotective Effects in Alzheimer's Disease by Switching Microglia M1/M2 Polarization Through PI3K-AKT Signaling.Physiological research · 2025Article
- Potential of Neuroinflammation-Modulating Strategies in Tuberculous Meningitis: Targeting Microglia.Aging and disease · 2024Review
- Interactions between CNS and immune cells in tuberculous meningitis.Frontiers in immunology · 2024Review
- The CB2-PKC pathway is involved in esketamine-induced anti-inflammation in BV-2 microglial cells exposed to lipopolysaccharides.American journal of translational research · 2024Article
- Exploring Chinese herbal medicine for ischemic stroke: insights into microglia and signaling pathways.Frontiers in pharmacology · 2024Review
- An Update on Protein Kinases as Therapeutic Targets-Part I: Protein Kinase C Activation and Its Role in Cancer and Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Progress towards Adjuvant Development: Focus on Antiviral Therapy.International journal of molecular sciences · 2023Review
- Icaritin inhibits neuroinflammation in a rat cerebral ischemia model by regulating microglial polarization through the GPER-ERK-NF-κB signaling pathway.Molecular medicine (Cambridge, Mass.) · 2022Article
- Review
- Enhanced immunogenicity of the tuberculosis subunit Rv0572c vaccine delivered in DMT liposome adjuvant as a BCG-booster.Tuberculosis (Edinburgh, Scotland) · 2022Article
- Activation of Three Major Signaling Pathways After Endurance Training and Spinal Cord Injury.Molecular neurobiology · 2022Article
- Glial-Neuronal Interactions in Pathogenesis and Treatment of Spinal Cord Injury.International journal of molecular sciences · 2021Review
- Design of Trehalose-Based Amide/Sulfonamide C-type Lectin Receptor Signaling Compounds.ChemMedChem · 2021Article
- Microglia Polarization in Alzheimer's Disease: Mechanisms and a Potential Therapeutic Target.Frontiers in aging neuroscience · 2021Review
- PAID study design on the role of PKC activation in immune/inflammation-related depression: a randomised placebo-controlled trial protocol.General psychiatry · 2021Article
- Aryl Trehalose Derivatives as Vaccine Adjuvants forJournal of medicinal chemistry · 2020Article
- PKC Mediates LPS-Induced IL-1β Expression and Participates in the Pro-inflammatory Effect of ANeurochemical research · 2019Article
- Inhibitory Effects of the Two Novel TSPO Ligands 2-Cl-MGV-1 and MGV-1 on LPS-induced Microglial Activation.Cells · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Microglial activation has long been recognized as a hallmark of neuroinflammation. Recently, the bacillus Calmette-Guerin (BCG) vaccine has been reported to exert neuroprotective effects against several neurodegenerative disorders. Trehalose-6,6'-dibehenate (TDB) is a synthetic analogue of trehalose-6,6'-dimycolate (TDM, also known as the mycobacterial cord factor) and is a new adjuvant of tuberculosis subunit vaccine currently in clinical trials. Both TDM and TDB can activate macrophages and dendritic cells through binding to C-type lectin receptor Mincle; however, its action mechanism in microglia and their relationship with neuroinflammation are still unknown. In this article, we found that TDB inhibited LPS-induced M1 microglial polarization in primary microglia and BV-2 cells. However, TDB itself had no effects on IKK, p38, and JNK activities or cytokine expression. In contrast, TDB activated ERK1/2 through PLC-γ1/PKC signaling and in turn decreased LPS-induced NF-κB nuclear translocation. Furthermore, TDB-induced AMPK activation via PLC-γ1/calcium/CaMKKβ-dependent pathway and thereby enhanced M2 gene expressions. Interestingly, knocking out Mincle did not alter the anti-inflammatory and M2 polarization effects of TDB in microglia. Conditional media from LPS-stimulated microglial cells can induce in vitro neurotoxicity, and this action was attenuated by TDB. Using a mouse neuroinflammation model, we found that TDB suppressed LPS-induced M1 microglial activation and sickness behavior, but promoted M2 microglial polarization in both WT and Mincle
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