ArticleJournal of neuroinflammation2022
MyD88-TLR4-dependent choroid plexus activation precedes perilesional inflammation and secondary brain edema in a mouse model of intracerebral hemorrhage.
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- Ginsenoside Rg2 attenuates secondary brain injury following intracerebral hemorrhage by inhibiting NLRP3-mediated pyroptosis.Journal of neuroinflammation · 2026Article
- The Role of Microglial Cells and Cytokine Modulation in Alzheimer's Disease: A Neuroinflammatory Perspective.Current Alzheimer research · 2026Review
- The immune-endothelial axis in neurovascular pathophysiology: a framework for targeted interventions.Frontiers in immunology · 2026Review
- [Predictive Performance of Routine Blood Test Parameters for the Severity of Brain Damage in Patients With Acute Cerebral Hemorrhage in High-Altitude Regions].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Article
- Choroid Plexus Fibroblast-ILC2 Niche Promotes Adult Hippocampal Neurogenesis after Traumatic Brain Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Perihematomal Neurovascular Protection: Blocking HSP90 Reduces Blood Infiltration Associated with Inflammatory Effects Following Intracerebral Hemorrhage in Rates.Translational stroke research · 2025Article
- miRNA506 Activates Sphk1 Binding with Sirt1 to Inhibit Brain Injury After Intracerebral Hemorrhage via PI3K/AKT Signaling Pathway.Molecular neurobiology · 2025Article
- Dual role of TLR4 in bacterial meningitis through regulating endothelial pyroptosis and inflammatory response during extraintestinal pathogenicFrontiers in immunology · 2025Article
- Astrocyte-microglia crosstalk in subarachnoid hemorrhage: mechanisms and treatments.Frontiers in immunology · 2025Review
- DIA-based proteomics reveals anti-inflammatory role of DL-3-Translational neuroscience · 2025Article
- C1-inhibitor to prevent intracerebral hemorrhage-related secondary brain injury.Fluids and barriers of the CNS · 2024Article
- Paclitaxel triggers molecular and cellular changes in the choroid plexus.Frontiers in pain research (Lausanne, Switzerland) · 2024Article
- A year in review: brain barriers and brain fluids research in 2022.Fluids and barriers of the CNS · 2023Article
- Transient ischemic stroke triggers sustained damage of the choroid plexus blood-CSF barrier.Frontiers in cellular neuroscience · 2023Article
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12 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThe functional neurological outcome of patients with intracerebral hemorrhage (ICH) strongly relates to the degree of secondary brain injury (ICH-SBI) evolving within days after the initial bleeding. Different mechanisms including the incitement of inflammatory pathways, dysfunction of the blood-brain barrier (BBB), activation of resident microglia, and an influx of blood-borne immune cells, have been hypothesized to contribute to ICH-SBI. Yet, the spatiotemporal interplay of specific inflammatory processes within different brain compartments has not been sufficiently characterized, limiting potential therapeutic interventions to prevent and treat ICH-SBI.
methodsWe used a whole-blood injection model in mice, to systematically characterized the spatial and temporal dynamics of inflammatory processes after ICH using 7-Tesla magnetic resonance imaging (MRI), spatial RNA sequencing (spRNAseq), functional BBB assessment, and immunofluorescence average-intensity-mapping.
resultsWe identified a pronounced early response of the choroid plexus (CP) peaking at 12-24 h that was characterized by inflammatory cytokine expression, epithelial and endothelial expression of leukocyte adhesion molecules, and the accumulation of leukocytes. In contrast, we observed a delayed secondary reaction pattern at the injection site (striatum) peaking at 96 h, defined by gene expression corresponding to perilesional leukocyte infiltration and correlating to the delayed signal alteration seen on MRI. Pathway analysis revealed a dependence of the early inflammatory reaction in the CP on toll-like receptor 4 (TLR4) signaling via myeloid differentiation factor 88 (MyD88). TLR4 and MyD88 knockout mice corroborated this observation, lacking the early upregulation of adhesion molecules and leukocyte infiltration within the CP 24 h after whole-blood injection.
conclusionsWe report a biphasic brain reaction pattern after ICH with a MyD88-TLR4-dependent early inflammatory response of the CP, preceding inflammation, edema and leukocyte infiltration at the lesion site. Pharmacological targeting of the early CP activation might harbor the potential to modulate the development of ICH-SBI.
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