ArticleJournal of neuroinflammation2007
Reactive oxygen species and p47phox activation are essential for the Mycobacterium tuberculosis-induced pro-inflammatory response in murine microglia.
Article in Journal of neuroinflammation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 75 citations in OpenAlex.
- Review
- Deubiquitinase USP15 restricts LC3-dependent targeting ofAutophagy · 2026Article
- SMURF2 inhibits autophagic control ofbioRxiv : the preprint server for biology · 2025Article
- Spatially heterogeneous lipid dysregulation in tuberculous meningitis.Neurobiology of disease · 2024Article
- Potential of Neuroinflammation-Modulating Strategies in Tuberculous Meningitis: Targeting Microglia.Aging and disease · 2024Review
- Insulin Mediates Lipopolysaccharide-Induced Inflammatory Responses and Oxidative Stress in BV2 Microglia.Journal of inflammation research · 2024Article
- Interactions between CNS and immune cells in tuberculous meningitis.Frontiers in immunology · 2024Review
- Article
- Ginsenoside Rc from Panax Ginseng Ameliorates Palmitate-Induced UB/OC-2 Cochlear Cell Injury.International journal of molecular sciences · 2023Article
- Affinity of Mycobacterium tuberculosis strains for M059K microglial cells after migration through A549 alveolar epithelium.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2021Article
- The pathogenesis of tuberculous meningitis.Journal of leukocyte biology · 2019Review
- Rv0646c, an esterase from M. tuberculosis, up-regulates the host immune response in THP-1 macrophages cells.Molecular and cellular biochemistry · 2018Article
- Infectious immunity in the central nervous system and brain function.Nature immunology · 2017Review
- Protective Effects and Possible Mechanisms of Ergothioneine and Hispidin against Methylglyoxal-Induced Injuries in Rat Pheochromocytoma Cells.Oxidative medicine and cellular longevity · 2017Article
- Microglia activation in a pediatric rabbit model of tuberculous meningitis.Disease models & mechanisms · 2016Article
- Does Concurrent Use of Some Botanicals Interfere with Treatment of Tuberculosis?Neuromolecular medicine · 2016Review
- MicroRNAs mediating CNS inflammation: Small regulators with powerful potential.Brain, behavior, and immunity · 2016Review
- Innate signaling mechanisms controlling Mycobacterium chelonae-mediated CCL2 and CCL5 expression in macrophages.Journal of microbiology (Seoul, Korea) · 2015Article
- Periodontal Disease-Induced Atherosclerosis and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2015Review
- Dieckol Attenuates Microglia-mediated Neuronal Cell Death via ERK, Akt and NADPH Oxidase-mediated Pathways.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2015Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundActivated microglia elicits a robust amount of pro-inflammatory cytokines, which are implicated in the pathogenesis of tuberculosis in the central nervous system (CNS). However, little is known about the intracellular signaling mechanisms governing these inflammatory responses in microglia in response to Mycobacterium tuberculosis (Mtb).
methodsMurine microglial BV-2 cells and primary mixed glial cells were stimulated with sonicated Mtb (s-Mtb). Intracellular ROS levels were measured by staining with oxidative fluorescent dyes [2',7'-Dichlorodihydrofluorescein diacetate (H2DCFDA) and dihydroethidium (DHE)]. NADPH oxidase activities were measured by lucigenin chemiluminescence assay. S-Mtb-induced MAPK activation and pro-inflammatory cytokine release in microglial cells were measured using by Western blot analysis and enzyme-linked immunosorbent assay, respectively.
resultsWe demonstrate that s-Mtb promotes the up-regulation of reactive oxygen species (ROS) and the rapid activation of mitogen-activated protein kinases (MAPKs), including p38 and extracellular signal-regulated kinase (ERK) 1/2, as well as the secretion of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-12p40 in murine microglial BV-2 cells and primary mixed glial cells. Both NADPH oxidase and mitochondrial electron transfer chain subunit I play an indispensable role in s-Mtb-induced MAPK activation and pro-inflammatory cytokine production in BV-2 cells and mixed glial cells. Furthermore, the activation of cytosolic NADPH oxidase p47phox and MAPKs (p38 and ERK1/2) is mutually dependent on s-Mtb-induced inflammatory signaling in murine microglia. Neither TLR2 nor dectin-1 was involved in s-Mtb-induced inflammatory responses in murine microglia.
conclusionThese data collectively demonstrate that s-Mtb actively induces the pro-inflammatory response in microglia through NADPH oxidase-dependent ROS generation, although the specific pattern-recognition receptors involved in these responses remain to be identified.
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