ArticleJournal of neuroinflammation2020
The prenatal challenge with lipopolysaccharide and polyinosinic:polycytidylic acid disrupts CX3CL1-CX3CR1 and CD200-CD200R signalling in the brains of male rat offspring: a link to schizophrenia-like behaviours.
Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Chemokine Dysregulation and Neuroinflammation in Schizophrenia: A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Microglia and neuroinflammation: function, heterogeneity, and crosstalk.Cellular & molecular immunology · 2026Review
- Placental and juvenile immune responses to maternal immune activation are differentially regulated by sex chromosomes and gonads across gestation.Journal of neuroinflammation · 2026Article
- Fractalkine (Chemokine CX3CL1) Signaling During Placentation and Placental Function.International journal of molecular sciences · 2026Review
- The Causal Relationships Between Inflammatory Proteins, Brain Structure, and Psychiatric Disorders: A Two-Step Mendelian Randomization Analysis.Schizophrenia bulletin · 2025Article
- Emerging role of neural stem/progenitor cell secretome in brain inflammatory response modulation.Pharmacological reports : PR · 2025Review
- Targeting CX3CR1 Signaling Dynamics: A Critical Determinant in the Temporal Regulation of Post-Stroke Neurorepair.Brain sciences · 2025Review
- Association between endogenous lactate accumulation and dysregulated activation of the NLRP3 inflammasome pathway in schizophrenia.Scientific reports · 2025Observational
- Interleukin-6 produces behavioral deficits in pre-pubescent mice independent of neuroinflammation.Brain, behavior, and immunity · 2025Article
- Maternal Immune Activation and Neurodevelopmental Disorders: Integrating Molecular, Cellular and Systems Mechanisms.Neuropsychiatric disease and treatment · 2025Review
- Article
- Neuron-Microglia Interaction is Involved in Anti-inflammatory Response by Vagus Nerve Stimulation in the Prefrontal Cortex of Rats Injected with Polyinosinic:Polycytidylic Acid.Molecular neurobiology · 2024Article
- The role of microglia in early neurodevelopment and the effects of maternal immune activation.Seminars in immunopathology · 2024Review
- Prenatal Immune Challenge Differentiates the Effect of Aripiprazole and Risperidone on CD200-CD200R and CX3CL1-CX3CR1 Dyads and Microglial Polarization: A Study in Organotypic Cortical Cultures.Life (Basel, Switzerland) · 2024Article
- Fetal brain response to maternal inflammation requires microglia.Development (Cambridge, England) · 2024Article
- Mendelian randomization analysis of causal and druggable circulating inflammatory proteins in schizophrenia.Frontiers in psychiatry · 2024Article
- CD200 in dentate gyrus improves depressive-like behaviors of mice through enhancing hippocampal neurogenesis via alleviation of microglia hyperactivation.Journal of neuroinflammation · 2023Article
- New Radiobiological Principles for the CNS Arising from Space Radiation Research.Life (Basel, Switzerland) · 2023Article
- Insights into the Potential Impact of Quetiapine on the Microglial Trajectory and Inflammatory Response in Organotypic Cortical Cultures Derived from Rat Offspring.Biomedicines · 2023Article
- Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThe bidirectional communication between neurons and microglia is fundamental for the homeostasis and biological function of the central nervous system. Maternal immune activation (MIA) is considered to be one of the factors affecting these interactions. Accordingly, MIA has been suggested to be involved in several neuropsychiatric diseases, including schizophrenia. The crucial regulatory systems for neuron-microglia crosstalk are the CX3CL1-CX3CR1 and CD200-CD200R axes.
methodsWe aimed to clarify the impact of MIA on CX3CL1-CX3CR1 and CD200-CD200R signalling pathways in the brains of male Wistar rats in early and adult life by employing two neurodevelopmental models of schizophrenia based on the prenatal challenge with lipopolysaccharide (LPS) and polyinosinic:polycytidylic acid (Poly I:C). We also examined the effect of MIA on the expression of microglial markers and the profile of cytokines released in the brains of young offspring, as well as the behaviour of adult animals. Moreover, we visualized the localization of ligand-receptor systems in the hippocampal regions (CA1, CA3 and DG) and the frontal cortex of young rats exposed to MIA. The differences between groups were analysed using Student's t test.
resultsWe observed that MIA altered developmental trajectories in neuron-microglia communication in the brains of young offspring, as evidenced by the disruption of CX3CL1-CX3CR1 and/or CD200-CD200R axes. Our data demonstrated the presence of abnormalities after LPS-induced MIA in levels of Cd40, Il-1β, Tnf-α, Arg1, Tgf-β and Il-10, as well as IBA1, IL-1β and IL-4, while after Poly I:C-generated MIA in levels of Cd40, iNos, Il-6, Tgf-β, Il-10, and IBA1, IL-1β, TNF-α, IL-6, TGF-β and IL-4 early in the life of male animals. In adult male rats that experienced prenatal exposure to MIA, we observed behavioural changes resembling a schizophrenia-like phenotype.
conclusionsOur study provides evidence that altered CX3CL1-CX3CR1 and/or CD200-CD200R pathways, emerging after prenatal immune challenge with LPS and Poly I:C, might be involved in the aetiology of schizophrenia.
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Registered trials
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