ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
Interleukin-1 influences ischemic brain damage in the mouse independently of the interleukin-1 type I receptor.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
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
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 144 citations in OpenAlex.
- Systematic Review and Meta-Analysis of the Efficacy of Interleukin-1 Receptor Antagonist in Animal Models of Stroke: an Update.Translational stroke research · 2016Pooled it
- Genomic and proteomic conversion of brain ischemia to Alzheimer's disease.Frontiers in cell and developmental biology · 2026Review
- Unexpectedly High and Difficult-to-Explain Regenerative Capacity in an 82-Year-Old Patient with Insulin-Requiring Type 2 Diabetes and End-Stage Renal Disease.Journal of clinical medicine · 2025Article
- Hemostatic Status of Neonates with Perinatal Hypoxia, Studied via NATEM in Cord Blood Samples.Children (Basel, Switzerland) · 2024Article
- IL-1β disrupts the initiation of blood-brain barrier development by inhibiting endothelial Wnt/β-catenin signaling.iScience · 2024Article
- What Is IL-1 for? The Functions of Interleukin-1 Across Evolution.Frontiers in immunology · 2022Article
- Post-Ischemic Neurodegeneration of the Hippocampus Resembling Alzheimer's Disease Proteinopathy.International journal of molecular sciences · 2021Review
- Spata2 Knockdown Exacerbates Brain Inflammation via NF-κB/P38MAPK Signaling and NLRP3 Inflammasome Activation in Cerebral Ischemia/Reperfusion Rats.Neurochemical research · 2021Article
- Role of microglial and endothelial CD36 in post-ischemic inflammasome activation and interleukin-1β-induced endothelial activation.Brain, behavior, and immunity · 2021Article
- Cytokines as therapeutic targets for cardio- and cerebrovascular diseases.Basic research in cardiology · 2021Review
- Participation of Amyloid and Tau Protein in Post-Ischemic Neurodegeneration of the Hippocampus of a Nature Identical to Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Cell-specific conditional deletion of interleukin-1 (IL-1) ligands and its receptors: a new toolbox to study the role of IL-1 in health and disease.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Neuroprotective Effects of Qingnao Dripping Pills Against Cerebral IschemiaFrontiers in pharmacology · 2020Article
- Polymorphism of Interleukin 1B May Modulate the Risk of Ischemic Stroke in Polish Patients.Medicina (Kaunas, Lithuania) · 2019Article
- Dual PPARα/γ agonist aleglitazar confers stroke protection in a model of mild focal brain ischemia in mice.Journal of molecular medicine (Berlin, Germany) · 2019Article
- Post-stroke inflammation-target or tool for therapy?Acta neuropathologica · 2019Review
- Influence of low-dose alcohol consumption on post-ischemic inflammation: Role of cystathionine γ-lyase.Alcohol (Fayetteville, N.Y.) · 2019Article
- Interleukin-1 mediates ischaemic brain injury via distinct actions on endothelial cells and cholinergic neurons.Brain, behavior, and immunity · 2019Article
- Chronic Mild Hyperhomocysteinemia Alters Inflammatory and Oxidative/Nitrative Status and Causes Protein/DNA Damage, as well as Ultrastructural Changes in Cerebral Cortex: Is Acetylsalicylic Acid Neuroprotective?Neurotoxicity research · 2018Article
- Inflammatory molecules might become both biomarkers and therapeutic targets for stroke management.Therapeutic advances in neurological disorders · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cytokine interleukin-1beta (IL-1beta) contributes to ischemic, excitotoxic, and traumatic brain injury. IL-1beta actions depend on interaction with a single receptor (IL-1RI), which associates with an accessory protein (IL-1RAcP), and is blocked by IL-1 receptor antagonist (IL-1ra). Here we show that in normal mice [wild-type (WT)], intracerebroventricular injection of IL-1ra markedly reduces (-50%; p < 0.01) ischemic brain damage caused by reversible occlusion of the middle cerebral artery, whereas injection of IL-1beta exacerbates damage (+45%; p < 0.05). Mice lacking IL-1RI [IL-1RI knock-out (KO)] exhibited ischemic brain damage that is almost identical to that of the WT (infarct volume 43.7 +/- 6.1 and 46.2 +/- 6.2 mm3, respectively), but failed to respond to injection of IL-1ra. However, injection of IL-1beta (intracerebroventricularly) exacerbated ischemic brain damage in IL-1RI KO (+61%; p < 0.001) and in WT mice (+45%). This effect of IL-1beta was abolished by heat denaturation in all animals, and was reversed by IL-1ra in WT, but not IL-1RI KO mice. In contrast, IL-1RI KO mice were completely resistant to effects of IL-1beta on food intake or body weight. IL-1RAcP mRNA was increased by stroke in WT, but reduced in IL-1RI KO mice compared with sham-operated mice. Type II IL-1 receptor mRNA was significantly increased 4 hr after ischemia in WT and IL-1RI KO (+20%) animals. These data show that IL-1beta can exacerbate ischemic brain damage independently of IL-1RI and suggest the existence of additional signaling receptor or receptors for IL-1 in the brain.
Indexed as
Identifiers
11756486PMC6757585W1885614951What OpenQuestion holds
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.