ArticleBiological research2024
Increased levels and activation of the IL-17 receptor in microglia contribute to enhanced neuroinflammation in cerebellum of hyperammonemic rats.
Article in Biological research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 13 citations in OpenAlex.
- The role of systemic inflammation in hepatic encephalopathy: advances in inflammatory mechanisms, prevention and treatment research.Annals of medicine · 2026Review
- Peripheral IL-17 Triggers, and anti-IL-17 Treatment Prevents, Neuroinflammation and Alterations in Neurotransmission in Hippocampus and Cognitive Impairment in Hyperammonemic Rats.Molecular neurobiology · 2026Article
- The IL-17A modulating astrocytic activity was associated with the electroacupuncture-mediated improvement of sensorimotor ability after stroke.Chinese medicine · 2026Article
- Encephalopathy: Cause, Pathogenesis, and Treatment.MedComm · 2026Review
- Cerebellar microglia-derived IL-17A mitigates autism-related behavioral and synaptic deficits.Molecular psychiatry · 2026Article
- Cang-Ai Volatile Oil Ameliorates Chronic Unpredictable Mild Stress-Induced Depression-like Symptoms in Rats by Regulating NT/Trk Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Enhancing Laying Hens' Egg Quality and Health with Se-Enriched Earthworm Hydrolysate.Biological trace element research · 2026Article
- Long-term rapamycin treatment suppresses IL-17-producing gamma delta T cells and blunts neuroinflammation in aging.PloS one · 2026Article
- Elevated Plasma BDNF in Early Primary Biliary Cholangitis: Associations with Liver Fibrosis, IL-6, IL-18, Fatigue, and Cognitive Impairment.International journal of molecular sciences · 2025Observational
- IL-17A mediates inflammation-related retinal pigment epithelial cells injuryInternational journal of ophthalmology · 2025Article
- The Role of Neuroinflammation in the Pathogenesis of Hepatic Encephalopathy.Journal of immunology research · 2025Review
- Network Pharmacology, Molecular Docking, Molecular Dynamics to Explore the Mechanism of Danggui Shaoyao Powder for Hepatic Encephalopathy.Current pharmaceutical design · 2025Article
- A transient blood IL-17 increase triggers neuroinflammation in cerebellum and motor incoordination in hyperammonemic rats.Journal of neuroinflammation · 2024Article
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5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundPatients with liver cirrhosis may show minimal hepatic encephalopathy (MHE) with mild cognitive impairment and motor incoordination. Rats with chronic hyperammonemia reproduce these alterations. Motor incoordination in hyperammonemic rats is due to increased GABAergic neurotransmission in cerebellum, induced by neuroinflammation, which enhances TNFα-TNFR1-S1PR2-CCL2-BDNF-TrkB pathway activation. The initial events by which hyperammonemia triggers activation of this pathway remain unclear. MHE in cirrhotic patients is triggered by a shift in inflammation with increased IL-17. The aims of this work were: (1) assess if hyperammonemia increases IL-17 content and membrane expression of its receptor in cerebellum of hyperammonemic rats; (2) identify the cell types in which IL-17 receptor is expressed and IL-17 increases in hyperammonemia; (3) assess if blocking IL-17 signaling with anti-IL-17 ex-vivo reverses activation of glia and of the TNFα-TNFR1-S1PR2-CCL2-BDNF-TrkB pathway.
resultsIL-17 levels and membrane expression of the IL-17 receptor are increased in cerebellum of rats with hyperammonemia and MHE, leading to increased activation of IL-17 receptor in microglia, which triggers activation of STAT3 and NF-kB, increasing IL-17 and TNFα levels, respectively. TNFα released from microglia activates TNFR1 in Purkinje neurons, leading to activation of NF-kB and increased IL-17 and TNFα also in these cells. Enhanced TNFR1 activation also enhances activation of the TNFR1-S1PR2-CCL2-BDNF-TrkB pathway which mediates microglia and astrocytes activation.
conclusionsAll these steps are triggered by enhanced activation of IL-17 receptor in microglia and are prevented by ex-vivo treatment with anti-IL-17. IL-17 and IL-17 receptor in microglia would be therapeutic targets to treat neurological impairment in patients with MHE.
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