ArticleNeurochemistry international2008
TNF is a key mediator of septic encephalopathy acting through its receptor, TNF receptor-1.
Article in Neurochemistry international, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.
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Who cites it
107 citing papers in PubMed, 1 synthesis or guideline pooled it, 223 citations in OpenAlex.
- The Key Drivers of Brain Injury by Systemic Inflammatory Responses after Sepsis: Microglia and Neuroinflammation.Molecular neurobiology · 2023Pooled it
- Transcutaneous electrical acupoint stimulation for prevention of postoperative delirium in geriatric patients with silent lacunar infarction: a preliminary study.Clinical interventions in aging · 2018Trial
- Endotoxemia-induced inflammation and the effect on the human brain.Critical care (London, England) · 2010Trial
- Cerebral perfusion in sepsis-associated delirium.Critical care (London, England) · 2008Trial
- The FDA-approved excipient N,N-dimethylacetamide improves survival and attenuates inflammatory pathways in a murine model of endotoxemia.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Article
- Neuroimmune Mechanisms Transforming Acute Injury to Long-Term Brain Dysfunction After Sepsis.Clinics in chest medicine · 2026Review
- Macrostructural, microstructural, and cellular effects of neuroinflammation on the mouse brain.Brain, behavior, & immunity - health · 2026Article
- Role of the intestinal microbiota in sepsis-associated encephalopathy.Burns & trauma · 2026Review
- Cetirizine and Dexamethasone in Sepsis: Insights into Maresin-1 Signaling and Cytokine Regulation.Journal of clinical medicine · 2025Article
- The missing link: TNF-α as a unifying mechanism in methamphetamine-induced neuronal dysfunction and blood-brain barrier compromise.Journal of neuroimmunology · 2025Review
- Dihydromyricetin protects hippocampal neurons in sepsis-associated encephalopathy by reducing ER stress-mediated apoptosis and inflammation.Journal of molecular histology · 2025Article
- Neuroinflammatory Mechanisms of Adult Sepsis-Associated Encephalopathy: Implications for Blood-Brain Barrier Disruption and Oxidative Stress.Diagnostics (Basel, Switzerland) · 2025Review
- Partial depletion of circulating neutrophil granulocytes in mice exacerbates the inflammatory response and hypothermia during LPS induced severe systemic inflammation.Frontiers in immunology · 2025Article
- Aquaporins in sepsis- an update.Frontiers in immunology · 2024Review
- Astrocyte regulation of extracellular space parameters across the sleep-wake cycle.Frontiers in cellular neuroscience · 2024Review
- Aquaporins: Potential Targets in Inflammatory Diseases.The Eurasian journal of medicine · 2023Article
- Role of Imaging Modalities andACS chemical neuroscience · 2023Article
- Paediatric sepsis-associated encephalopathy (SAE): a comprehensive review.Molecular medicine (Cambridge, Mass.) · 2023Review
- Andrographolide Attenuates Inflammation Due to Intra-Abdominal Sepsis by Enhancing Bacterial Clearance in Mice.Journal of inflammation research · 2023Article
- The Many Faces of Astrocytes in the Septic Brain.Molecular neurobiology · 2022Review
47 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
5 authors at 1 institution in 1 country.
Funding
Abstract
In this study, we demonstrate that mice deficient in TNFR1 (TNFR1(-/-)) were resistant to LPS-induced encephalopathy. Systemic administration of lipopolysaccharide (LPS) induces a widespread inflammatory response similar to that observed in sepsis. Following LPS administration TNFR1(-/-) mice had less caspase-dependent apoptosis in brain cells and fewer neutrophils infiltrating the brain (p<0.039), compared to control C57Bl6 (TNFR1(+/+)) mice. TNFR1-dependent increase in aquaporin (AQP)-4 mRNA and protein expression was observed with a concomitant increase in water content, in brain (18% increase in C57Bl6 mice treated with LPS versus those treated with saline), similar to cerebral edema observed in sepsis. Furthermore, absence of TNFR1 partially but significantly reduced the activation of astrocytes, as shown by immunofluorescence and markedly inhibited iNOS mRNA expression (p<0.01). Septic encephalopathy is a devastating complication of sepsis. Although, considerable work has been done to identify the mechanism causing the pathological alterations in this setting, the culprit still remains an enigma. Our results demonstrate for the first time that endotoxemia leads to inflammation in brain, with alteration in blood-brain barrier, up-regulation of AQP4 and associated edema, neutrophil infiltration, astrocytosis, as well as apoptotic cellular death, all of which appear to be mediated by TNF-alpha signaling through TNFR1.
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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.