ArticleLipids in health and disease2023
HDL and LDL have distinct, opposing effects on LPS-induced brain inflammation.
Article in Lipids in health and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- A Potential Link Between Dyslipidemia and Inflammation in Patients with Schizophrenia: Insights from Sterols and HDL Profile Analysis.International journal of molecular sciences · 2026Article
- NicheProt: Cell-type-resolved proteomics of tissue compartments.Science advances · 2026Article
- Plasma Lipoproteins as Key Regulators in Neuropathic Pain: A Comprehensive Review of Mechanisms and Clinical Potential.Pain and therapy · 2026Review
- Liver-nervous system axis: pathways, dysregulation, and translational perspectives.Journal of neuroinflammation · 2026Review
- Microbiota-Gut-Brain Axis Disruption, Neuroinflammation, and Potential Antioxidant-Based Treatments in Metabolic Diseases.Antioxidants (Basel, Switzerland) · 2026Review
- Metabolic phenotyping of sepsis in large multicenter cohorts: identification of a reproducible high-risk subgroup.Lipids in health and disease · 2026Article
- Regulatory Genomic Circuitry of Brain Age by Integrative Functional Genomic Analyses.Genomics, proteomics & bioinformatics · 2025Article
- Article
- Plasma apolipoproteins and memory function in alcohol use disorder: Findings in male C57BL/6J mice and men suggest a role for APOAI.Alcohol, clinical & experimental research · 2025Article
- Relevance of Lipoprotein Composition in Endothelial Dysfunction and the Development of Hypertension.International journal of molecular sciences · 2025Review
- Blood Lipid Levels and the Severity of Guillain-Barré Syndrome: A Single-Center Retrospective Cohort Study.Neurology research international · 2025Article
- Role of Oxidative Stress in Blood-Brain Barrier Disruption and Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- The Causal Relationship Between Choline Metabolites and Acute Acalculous Cholecystitis: IdentifyingNutrients · 2024Article
- Bidirectional two-sample mendelian randomization analysis identifies causal associations of MRI-based cortical thickness and surface area relation to NAFLD.Lipids in health and disease · 2024Article
- Unique pathways downstream of TLR-4 and TLR-7 activation: sex-dependent behavioural, cytokine, and metabolic consequences.Frontiers in cellular neuroscience · 2024Article
- Lipopolysaccharide triggers exacerbated microglial activation, excessive cytokine release and behavioural disturbances in mice with truncated Fused-in-Sarcoma Protein (FUS).Brain, behavior, & immunity - health · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endotoxemia and sepsis induce neuroinflammation and increase the risk of neurodegenerative disorders although the mechanism by which peripheral infection leads to brain inflammation is not well understood. While circulating serum lipoproteins are known immunometabolites with the potential to modulate the acute phase response and cross the blood brain barrier, their contribution to neuroinflammation during systemic infection is unknown. The objective of this study was to elucidate the mechanisms by which lipoprotein subclasses modulate lipopolysaccharide (LPS)-induced neuroinflammation. Adult C57BL/6 mice were divided into 6 treatment groups, including a sterile saline vehicle control group (n = 9), an LPS group (n = 11), a premixed LPS + HDL group (n = 6), a premixed LPS + LDL group (n = 5), a HDL only group (n = 6) and an LDL only group (n = 3). In all cases injections were administered intraperitoneally. LPS was administered at 0.5 mg/kg, and lipoproteins were administered at 20 mg/kg. Behavioural testing and tissue collection was performed 6 h post-injection. The magnitude of peripheral and central inflammation was determined by qPCR of pro-inflammatory genes in fresh liver and brain. Metabolite profiles of liver, plasma and brain were determined by
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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.