ArticleJournal of immunology (Baltimore, Md. : 1950)2016
Inducible Expression of CXCL1 within the Central Nervous System Amplifies Viral-Induced Demyelination.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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
27 citing papers in PubMed, 41 citations in OpenAlex.
- Acute viral encephalitis impacts dense-core amyloid plaque pathology and dysregulates myeloid responses to amyloid plaques.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Microglial-Derived IGF-1 Serves as a Regulator for Neuroimmune Homeostasis During Viral-Induced Demyelination.Viruses · 2026Article
- Cystatin F attenuates neuroinflammation and demyelination following murine coronavirus infection of the central nervous system.Journal of neuroinflammation · 2024Article
- The Role of Neutrophils in Multiple Sclerosis and Ischemic Stroke.Brain sciences · 2024Review
- Daphnetin alleviates neuropathic pain in chronic constrictive injury ratsPharmaceutical biology · 2023Article
- Article
- Sustained Infiltration of Neutrophils Into the CNS Results in Increased Demyelination in a Viral-Induced Model of Multiple Sclerosis.Frontiers in immunology · 2022Article
- Evaluating the role of chemokines and chemokine receptors involved in coronavirus infection.Expert review of clinical immunology · 2022Article
- Molecular Mechanisms of SARS-CoV-2/COVID-19 Pathogenicity on the Central Nervous System: Bridging Experimental Probes to Clinical Evidence and Therapeutic Interventions.Advances in experimental medicine and biology · 2022Review
- Single-Cell RNA Sequencing Reveals the Diversity of the Immunological Landscape following Central Nervous System Infection by a Murine Coronavirus.Journal of virology · 2020Article
- Candesartan could ameliorate the COVID-19 cytokine storm.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2020Article
- Article
- Astrocyte- and Neuron-Derived CXCL1 Drives Neutrophil Transmigration and Blood-Brain Barrier Permeability in Viral Encephalitis.Cell reports · 2020Article
- CXCR2 Signaling and Remyelination in Preclinical Models of Demyelination.DNA and cell biology · 2020Review
- The role of neutrophils in neuro-immune modulation.Pharmacological research · 2020Review
- Disrupted CXCR2 Signaling in Oligodendroglia Lineage Cells Enhances Myelin Repair in a Viral Model of Multiple Sclerosis.Journal of virology · 2019Article
- The microbiota protects from viral-induced neurologic damage through microglia-intrinsic TLR signaling.eLife · 2019Article
- T cell-selective deletion of Oct1 protects animals from autoimmune neuroinflammation while maintaining neurotropic pathogen response.Journal of neuroinflammation · 2019Article
- Deficiency of Socs3 leads to brain-targeted EAE via enhanced neutrophil activation and ROS production.JCI insight · 2019Article
- Innate Immune Responses and Viral-Induced Neurologic Disease.Journal of clinical medicine · 2018Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The functional role of the ELR(+) chemokine CXCL1 in host defense and disease following infection of the CNS with the neurotropic JHM strain of mouse hepatitis virus (JHMV) was examined. Mice in which expression of CXCL1 is under the control of a tetracycline-inducible promoter active within glial fibrillary acidic protein-positive cells were generated and this allowed for selectively increasing CNS expression of CXCL1 in response to JHMV infection and evaluating the effects on neuroinflammation, control of viral replication, and demyelination. Inducible expression of CNS-derived CXCL1 resulted in increased levels of CXCL1 protein within the serum, brain, and spinal cord that correlated with increased frequency of Ly6G(+)CD11b(+) neutrophils present within the CNS. Elevated levels of CXCL1 did not influence the generation of virus-specific T cells, and there was no difference in control of JHMV replication compared with control mice, indicating that T cell infiltration into the CNS is CXCL1-independent. Sustained CXCL1 expression within the CNS resulted in increased mortality that correlated with elevated neutrophil infiltration, diminished numbers of mature oligodendrocytes, and an increase in the severity of demyelination. Neutrophil ablation in CXCL1-transgenic mice reduced the severity of demyelination in mice, arguing for a role for these cells in white matter damage. Collectively, these findings illustrate that sustained CXCL1 expression amplifies the severity of white matter damage and that neutrophils can contribute to this process in a model of viral-induced neurologic disease.
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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.