ArticleCritical care (London, England)2010
The impact of IL-1 modulation on the development of lipopolysaccharide-induced cognitive dysfunction.
Article in Critical care (London, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers, 2 of them syntheses that pooled it.
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Who cites it
125 citing papers in PubMed, 2 syntheses or guidelines pooled it, 220 citations in OpenAlex.
- The Key Drivers of Brain Injury by Systemic Inflammatory Responses after Sepsis: Microglia and Neuroinflammation.Molecular neurobiology · 2023Pooled it
- Systemic inflammation and microglial activation: systematic review of animal experiments.Journal of neuroinflammation · 2015Pooled it
- Paternal cytokine administration alters sperm small ncRNAs and offspring brain and behavior.Molecular psychiatry · 2026Article
- Postoperative Impairment of GluA2 Ttrafficking in CA3 Induces Memory Consolidation Deficits in Aged Mice by Disrupting SPW-R in CA1.Journal of molecular neuroscience : MN · 2026Article
- Hippocampal cytopathology orchestrates post-septic cognitive dysfunction.Metabolic brain disease · 2026Review
- The FDA-approved excipient N,N-dimethylacetamide improves survival and attenuates inflammatory pathways in a murine model of endotoxemia.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Article
- Gut-brain axis and post-operative cognitive dysfunction: A multifactorial perspective on microbiota, inflammation, and cognitive health.World journal of gastrointestinal pharmacology and therapeutics · 2026Review
- Hydralazine Attenuates Lipopolysaccharide-Induced Murine Myocardial Dysfunction by Inhibition of Semicarbazide-Sensitive Amine Oxidase.Antioxidants (Basel, Switzerland) · 2025Article
- Increased Synapse Elimination by Inflammatory Cells Contributes to Long-lasting Post-Stroke Memory Dysfunction in Old Mice.bioRxiv : the preprint server for biology · 2025Article
- Convergence of sepsis-associated encephalopathy pathogenesis onto microglia.Journal of translational medicine · 2025Review
- Sepsis-Associated Brain Dysfunction: Mechanisms, Clinical Insights, and Therapeutic Strategies.Current drug targets · 2025Review
- Microglia in the aged brain develop a hypoactive molecular phenotype after surgery.Journal of neuroinflammation · 2024Article
- Physcion Mitigates LPS-Induced Neuroinflammation, Oxidative Stress, and Memory Impairments via TLR-4/NF-кB Signaling in Adult Mice.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Modulating neuroinflammation and cognitive function in postoperative cognitive dysfunction via CCR5-GPCRs-Ras-MAPK pathway targeting with microglial EVs.CNS neuroscience & therapeutics · 2024Article
- Retinal response to systemic inflammation differs between sexes and neurons.Frontiers in immunology · 2024Article
- Fish oil omega-3 Fatty Acids Alleviate Postoperative delirium-like Behavior in aged mice by Attenuating Neuroinflammation and Oxidative Stress.Neurochemical research · 2024Article
- Advances in the Understanding of the Correlation Between Neuroinflammation and Microglia in Alzheimer's Disease.ImmunoTargets and therapy · 2024Review
- IL-1β, the first piece to the puzzle of sepsis-related cognitive impairment?Frontiers in neuroscience · 2024Review
- Microglial Activation: Key Players in Sepsis-Associated Encephalopathy.Brain sciences · 2023Review
- Interplay between Systemic Glycemia and Neuroprotective Activity of Resveratrol in Modulating Astrocyte SIRT1 Response to Neuroinflammation.International journal of molecular sciences · 2023Article
65 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe impact of pro-inflammatory cytokines on neuroinflammation and cognitive function after lipopolysaccharide (LPS) challenge remains elusive. Herein we provide evidence that there is a temporal correlation between high-mobility group box 1 (HMGB-1), microglial activation, and cognitive dysfunction. Disabling the interleukin (IL)-1 signaling pathway is sufficient to reduce inflammation and ameliorate the disability.
methodsEndotoxemia was induced in wild-type and IL-1R-/- mice by intra peritoneal injection of E. Coli LPS (1 mg/kg). Markers of inflammation were assessed both peripherally and centrally, and correlated to behavioral outcome using trace fear conditioning.
resultsIncrease in plasma tumor necrosis factor-alpha (TNFalpha) peaked at 30 minutes after LPS challenge. Up-regulation of IL-1beta, IL-6 and HMGB-1 was more persistent, with detectable levels up to day three. A 15-fold increase in IL-6 and a 6.5-fold increase in IL-1beta mRNA at 6 hours post intervention (P < 0.001 respectively) was found in the hippocampus. Reactive microgliosis was observed both at days one and three, and was associated with elevated HMGB-1 and impaired memory retention (P < 0.005). Preemptive administration of IL-1 receptor antagonist (IL-1Ra) significantly reduced plasma cytokines and hippocampal microgliosis and ameliorated cognitive dysfunction without affecting HMGB-1 levels. Similar results were observed in LPS-challenged mice lacking the IL-1 receptor to those seen in LPS-challenged wild type mice treated with IL-1Ra.
conclusionsThese data suggest that by blocking IL-1 signaling, the inflammatory cascade to LPS is attenuated, thereby reducing microglial activation and preventing the behavioral abnormality.
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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.