ArticleJournal of neuroinflammation2019
CCL20-CCR6 axis modulated traumatic brain injury-induced visual pathologies.
Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Integrating multi-omics and machine learning to uncover CCL20 as a potential regulator of the immunosuppressive microenvironment in lung adenocarcinoma.Frontiers in immunology · 2026Article
- Eyes Are the Windows to the Soul: Reviewing the Possible Use of the Retina to Indicate Traumatic Brain Injury.International journal of molecular sciences · 2025Review
- Article
- Zinc signaling controls astrocyte-dependent synapse modulation via the PAF receptor pathway.Journal of neurochemistry · 2025Article
- Visual Impairment in Pre-Clinical Models of Mild Traumatic Brain Injury.Journal of neurotrauma · 2024Review
- Blast injury: Impact to the cornea.Experimental eye research · 2024Review
- Complement propagates visual system pathology following traumatic brain injury.Journal of neuroinflammation · 2024Article
- CC Chemokine Family Members' Modulation as a Novel Approach for Treating Central Nervous System and Peripheral Nervous System Injury-A Review of Clinical and Experimental Findings.International journal of molecular sciences · 2024Review
- Fentanyl dysregulates neuroinflammation and disrupts blood-brain barrier integrity in HIV-1 Tat transgenic mice.Journal of neurovirology · 2024Article
- Expression levels and clinical significance of serum miR-19a/CCL20 in patients with acute cerebral infarction.Open medicine (Warsaw, Poland) · 2024Article
- Spotlight on pro-inflammatory chemokines: regulators of cellular communication in cognitive impairment.Frontiers in immunology · 2024Review
- Lifelong Chronic Sleep Disruption in a Mouse Model of Traumatic Brain Injury.Neurotrauma reports · 2024Article
- Patients with Chronic Spinal Cord Injury Display a Progressive Alteration over the Years of the Activation Stages of the T Lymphocyte Compartment.International journal of molecular sciences · 2023Article
- Window into the mind: Advanced handheld spectroscopic eye-safe technology for point-of-care neurodiagnostic.Science advances · 2023Article
- Human amnionic progenitor cell secretome mitigates the consequence of traumatic optic neuropathy in a mouse model.Molecular therapy. Methods & clinical development · 2023Article
- Multispectral optoacoustic tomography (MSOT): Monitoring neurovascular changes in a mouse repetitive traumatic brain injury model.Journal of neuroscience methods · 2023Article
- Identification of immune associated potential molecular targets in proliferative diabetic retinopathy.BMC ophthalmology · 2023Article
- Blockade on Lin28a Prevents Cognitive Impairment and Disruption of the Blood-Brain Barrier Induced by Chronic Cerebral Hypoperfusion.Biomedicines · 2022Article
- CCL20/CCR6 Mediated Macrophage Activation and Polarization Can Promote Adenoid Epithelial Inflammation in Adenoid Hypertrophy.Journal of inflammation research · 2022Article
- Ischemic stroke: From pathological mechanisms to neuroprotective strategies.Frontiers in neurology · 2022Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundTraumatic brain injury (TBI) is a major cause of death and disability in the USA and the world; it constitutes 30% of injury-related deaths (Taylor et al., MMWR Surveill Summ 66:1-16, 2017). Contact sports athletes often experience repetitive TBI (rTBI), which exerts a cumulative effect later in life. Visual impairment is a common after-effect of TBI. Previously, we have shown that C-C chemokine 20 (CCL20) plays a critical role in neurodegeneration and inflammation following TBI (Das et al., J Neuroinflammation 8:148, 2011). C-C chemokine receptor 6 (CCR6) is the only receptor that CCL20 interacts with. The objective of the present study was to investigate the role of CCL20-CCR6 axis in mediating rTBI-induced visual dysfunction (TVD).
methodsWild type (WT) or CCR6 knock out (CCR6-/-) mice were subjected to closed head rTBI. Pioglitazone (PG) is a peroxisome proliferator-activated receptor γ (PPARγ) agonist which downregulates CCL20 production. Subsets of WT mice were treated with PG following final rTBI. A subset of mice was also treated with anti-CCL20 antibody to neutralize the CCL20 produced after rTBI. Histopathological assessments were performed to show cerebral pathologies, retinal pathologies, and inflammatory changes induced by rTBI.
resultsrTBI induced cerebral neurodegeneration, retinal degeneration, microgliosis, astrogliosis, and CCL20 expression. CCR6-/- mice showed reduced retinal degeneration, microgliosis, and inflammation. Treatment with CCL20 neutralization antibody or PG showed reduced CCL20 expression along with reduced retinal degeneration and inflammation. rTBI-induced GFAP-positive glial activation in the optic nerve was not affected by knocking out CCR6.
conclusionThe present data indicate that rTBI-induced retinal pathology is mediated at least in part by CCL20 in a CCR6-dependent manner.
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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.