ArticleAmerican journal of physiology. Cell physiology2008
Neuroinflammation facilitates LIF entry into brain: role of TNF.
Article in American journal of physiology. Cell physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 77 citations in OpenAlex.
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- Association between preoperative albumin levels and postoperative delirium in geriatric hip fracture patients.Frontiers in medicine · 2024Article
- An Integrative Approach to the Current Treatment of HIV-Associated Neurocognitive Disorders and the Implementation of Leukemia Inhibitor Factor as a Mediator of Neurocognitive Preservation.Life (Basel, Switzerland) · 2023Review
- Concordant and Discordant Cerebrospinal Fluid and Plasma Cytokine and Chemokine Responses in Mild Cognitive Impairment and Early-Stage Alzheimer's Disease.Biomedicines · 2023Article
- Selective visuoconstructional impairment following mild COVID-19 with inflammatory and neuroimaging correlation findings.Molecular psychiatry · 2023Article
- New insights intoFrontiers in cellular and infection microbiology · 2022Review
- Altered serum and cerebrospinal fluid TNF-α, caspase 3, and IL 1β in COVID-19 disease.Caspian journal of internal medicine · 2022Article
- Review
- The role of TNF-α in chordoma progression and inflammatory pathways.Cellular oncology (Dordrecht, Netherlands) · 2019Article
- Efficacy of leukemia inhibitory factor as a therapeutic for permanent large vessel stroke differs among aged male and female rats.Brain research · 2019Article
- Gut Inflammation in Association With Pathogenesis of Parkinson's Disease.Frontiers in molecular neuroscience · 2019Review
- Prenatal Programming of Neuroendocrine System Development by Lipopolysaccharide: Long-Term Effects.International journal of molecular sciences · 2018Review
- Neurovascular unit crosstalk: Pericytes and astrocytes modify cytokine secretion patterns of brain endothelial cells.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Article
- Neuroimmune Axes of the Blood-Brain Barriers and Blood-Brain Interfaces: Bases for Physiological Regulation, Disease States, and Pharmacological Interventions.Pharmacological reviews · 2018Review
- Lipopolysaccharide-Induced Striatal Nitrosative Stress and Impaired Social Recognition Memory Are Not Magnified by Paraquat Coexposure.Neurochemical research · 2018Article
- Blood vitronectin is a major activator of LIF and IL-6 in the brain through integrin-FAK and uPAR signaling.Journal of cell science · 2018Article
- Leukemia Inhibitory Factor-Loaded Nanoparticles with Enhanced Cytokine Metabolic Stability and Anti-Inflammatory Activity.Pharmaceutical research · 2018Article
- Integrative Computational Network Analysis Reveals Site-Specific Mediators of Inflammation in Alzheimer's Disease.Frontiers in physiology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Leukemia inhibitory factor (LIF) is a proinflammatory cytokine mediating a variety of central nervous system (CNS) responses to inflammatory stimuli. During lipopolysaccharide (LPS)-induced inflammation, blood concentrations of LIF increase, correlating with lethality of sepsis. Circulating LIF crosses the blood-brain barrier (BBB) by a saturable transport system. Here we determine how this transport system is regulated in neuroinflammation. Using transport assays that quantify the influx rate and volume of distribution of LIF in mice, we show that LPS facilitated the permeation of LIF from the blood to the brain without compromising the paracellular permeability of the BBB as determined by coadministration of fluorescein. Concurrently, gp130 (shared by the interleukin-6 family of cytokines), but not gp190 (the specific receptor for LIF) or cilliary neutrophic factor (CNTF-Ralpha, a unique receptor for cilliary neurotrophic factor that also uses gp130 and gp190), showed increased levels of mRNA and protein expression in cerebral microvessels from the LPS-treated mice. The upregulation of gp130 by LPS was at least partially mediated by vascular tumor necrosis factor receptor (TNFR)1 and TNFR2. This was shown by elevated TNFR1 and TNFR2 mRNA and protein in cerebral microvessels after LPS and by the absence of the LPS effect on gp130 in knockout mice lacking these receptors. The results show that neuroinflammation by LPS induces endothelial signaling and enhances cytokine transport across the BBB.
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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.