ArticlePloS one2021
Modulation of inflammatory responses by fractalkine signaling in microglia.
Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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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
17 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- Differential brain neuroimmune profiles and altered immune balance in autism spectrum disorder compared with psychotic disorder and neurotypical controls.Research square · 2026Article
- Microglia surveillance is directed toward neuron activation during sustained intracortical microstimulation.Journal of neural engineering · 2026Article
- The Fractalkine (FKN/CX3CL1) Pathway in Depression: A Critical Review of Its Role in Neuroinflammation and Therapeutic Potential.Neuropsychiatric disease and treatment · 2026Review
- Neurosteroid [3α,5α]-3-Hydroxy-pregnan-20-one Enhances the CX3CL1-CX3CR1 Pathway in the Brain of Alcohol-Preferring Rats with Sex-Specificity.Life (Basel, Switzerland) · 2024Article
- Dysregulated NFrontiers of medicine · 2024Article
- Altered response to Toll-like receptor 4 activation in fibromyalgia: A low-dose, human experimental endotoxemia pilot study.Brain, behavior, & immunity - health · 2023Article
- The Role of Fractalkine in the Regulation of Endometrial Iron Metabolism in Iron Deficiency.International journal of molecular sciences · 2023Article
- Fractalkine enhances oligodendrocyte regeneration and remyelination in a demyelination mouse model.Stem cell reports · 2023Article
- Age-dependent changes on fractalkine forms and their contribution to neurodegenerative diseases.Frontiers in molecular neuroscience · 2023Review
- Effects of Stromal Cell Conditioned Medium and Antipurinergic Treatment on Macrophage Phenotype.Tissue engineering. Part C, Methods · 2022Article
- Microglia and Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Potential significance of CX3CR1 dynamics in stress resilience against neuronal disorders.Neural regeneration research · 2022Review
- Heterozygous expression of the Alzheimer's disease-protective PLCγ2 P522R variant enhances Aβ clearance while preserving synapses.Cellular and molecular life sciences : CMLS · 2022Article
- Review
- Microglial cell response in α7 nicotinic acetylcholine receptor-deficient mice after systemic infection with Escherichia coli.Journal of neuroinflammation · 2022Article
- Ischemic Preconditioning Modulates the Peripheral Innate Immune System to Promote Anti-Inflammatory and Protective Responses in Mice Subjected to Focal Cerebral Ischemia.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive microglia are suggested to be involved in neurological disorders, and the mechanisms underlying microglial activity may provide insights into therapeutic strategies for neurological diseases. Microglia produce immunological responses to various stimuli, which include fractalkine (FKN or CX3CL1). CX3CR1, a FKN receptor, is present in microglial cells, and when FKN is applied before lipopolysaccharide (LPS) administration, LPS-induced inflammatory responses are inhibited, suggesting that the activation of the FKN signal is beneficial. Considering the practical administration for treatment, we investigated the influence of FKN on immunoreactive microglia using murine primary microglia and BV-2, a microglial cell line. The administration of LPS leads to nitric oxide (NO) production. NO was reduced when FKN was administered 4 h after LPS administration without a change in inducible nitric oxide synthase expression. In contrast, morphological changes, migratory activity, and proliferation were not altered by delayed FKN treatment. LPS decreases the CX3CR1 mRNA concentration, and the overexpression of CX3CR1 restores the FKN-mediated decrease in NO. CX3CR1 overexpression decreased the NO production that is mediated by LPS even without the application of FKN. ATP and ethanol also reduced CX3CR1 mRNA concentrations. In conclusion, the delayed FKN administration modified the LPS-induced microglial activation. The FKN signals were attenuated by a reduction in CX3CR1 by some inflammatory stimuli, and this modulated the inflammatory response of microglial cells, at least partially.
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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.