ArticleFrontiers in molecular neuroscience2016
Molecular Mechanisms Regulating LPS-Induced Inflammation in the Brain.
Article in Frontiers in molecular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- Review of OxLDL Driven Inflammatory Cell Activation.Current atherosclerosis reports · 2025Pooled it
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- 10-epi-Protectin DX and Resolvin D5International journal of molecular sciences · 2026Article
- Fructooligosaccharide ameliorates inflammation-induced chronic pain via deactivation of LPS/TLR-4/NF-κB p65/TNF-α/IL-6 pathway in estrogen-deficient rats.Inflammopharmacology · 2026Article
- Low-dose lipopolysaccharide pretreatment enhanced the proliferation and antibacterial activity of human adipose-derived mesenchymal stem cells.Regenerative therapy · 2026Article
- Pyridostigmine Attenuated Placental Ischemia-Upregulated Paraventricular Nucleus TLR4-Associated Hypertension in Preeclamptic Rats.Molecular neurobiology · 2026Article
- Probenecid relieves LPS-induced neuroinflammation by modulating the NLRP1 inflammasome pathway in BV2 cells.Scientific reports · 2025Article
- Ion Currents Mediated by TRPA1 Channels in Freshly Dissociated Rat Articular Chondrocytes: Biophysical Properties and Regulation by Inflammatory Processes.Pharmaceuticals (Basel, Switzerland) · 2025Article
- A comprehensive analysis of allele-specific expression and transcriptomic profiling in pig limbic and endocrine tissues.Frontiers in molecular neuroscience · 2025Article
- Bacterial endotoxin-lipopolysaccharide role in inflammatory diseases: An overview.Iranian journal of basic medical sciences · 2025Review
- TLR4-mediated chronic neuroinflammation has no effect on tangle pathology in a tauopathy mouse model.Frontiers in aging neuroscience · 2024Article
- Ellagic Acid Prevented Dextran-Sodium-Sulfate-Induced Colitis, Liver, and Brain Injury through Gut Microbiome Changes.Antioxidants (Basel, Switzerland) · 2023Article
- Transient disruption of functional connectivity and depression of neural fluctuations in a mouse model of acute septic encephalopathy.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- Microfluidic/HPLC combination to study carnosine protective activity on challenged human microglia: Focus on oxidative stress and energy metabolism.Frontiers in pharmacology · 2023Article
- HFrontiers in chemistry · 2023Review
- Article
- Dexmedetomidine Restores Autophagic Flux, Modulates Associated microRNAs and the Cholinergic Anti-inflammatory Pathway upon LPS-Treatment in Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2022Article
- Synthetic amyloid beta does not induce a robust transcriptional response in innate immune cell culture systems.Journal of neuroinflammation · 2022Article
- Article
- Manipulation of the diet-microbiota-brain axis in Alzheimer's disease.Frontiers in neuroscience · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Neuro-inflammation, one of the pathogenic causes of neurodegenerative diseases, is regulated through the cholinergic anti-inflammatory pathway via the α7 nicotinic acetylcholine receptor (α7 nAChR). We previously showed that either bacterial lipopolysaccharide (LPS) or immunization with the α7(1-208) nAChR fragment decrease α7 nAChRs density in the mouse brain, exacerbating chronic inflammation, beta-amyloid accumulation and episodic memory decline, which mimic the early stages of Alzheimer's disease (AD). To study the molecular mechanisms underlying the LPS and antibody effects in the brain, we employed an in vivo model of acute LPS-induced inflammation and an in vitro model of cultured glioblastoma U373 cells. Here, we report that LPS challenge decreased the levels of α7 nAChR RNA and protein and of acetylcholinesterase (AChE) RNA and activity in distinct mouse brain regions, sensitized brain mitochondria to the apoptogenic effect of Ca(2+) and modified brain microRNA profiles, including the cholinergic-regulatory CholinomiRs-132/212, in favor of anti-inflammatory and pro-apoptotic ones. Adding α7(1-208)-specific antibodies to the LPS challenge prevented elevation of both the anti-inflammatory and pro-apoptotic miRNAs while supporting the resistance of brain mitochondria to Ca(2+) and maintaining α7 nAChR/AChE decreases. In U373 cells, α7-specific antibodies and LPS both stimulated interleukin-6 production through the p38/Src-dependent pathway. Our findings demonstrate that acute LPS-induced inflammation induces the cholinergic anti-inflammatory pathway in the brain, that α7 nAChR down-regulation limits this pathway, and that α7-specific antibodies aggravate neuroinflammation by inducing the pro-inflammatory interleukin-6 and dampening anti-inflammatory miRNAs; however, these antibodies may protect brain mitochondria and decrease the levels of pro-apoptotic miRNAs, preventing LPS-induced neurodegeneration.
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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.