ArticleProceedings of the National Academy of Sciences of the United States of America2016
Infiltrating monocytes promote brain inflammation and exacerbate neuronal damage after status epilepticus.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 224 papers, 1 of them a synthesis that pooled it.
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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
224 citing papers in PubMed, 1 synthesis or guideline pooled it, 346 citations in OpenAlex.
- Neutrophil to Lymphocyte Ratio in Epilepsy: A Systematic Review.Mediators of inflammation · 2022Pooled it
- Effect of Probiotic Bifidobacterium breve in Improving Cognitive Function and Preventing Brain Atrophy in Older Patients with Suspected Mild Cognitive Impairment: Results of a 24-Week Randomized, Double-Blind, Placebo-Controlled Trial.Journal of Alzheimer's disease : JAD · 2022Trial
- Review
- Longitudinal analysis reveals myeloid cell contributions to murine neuroPASC pathogenesis.Nature communications · 2026Article
- Anti-Inflammatory and Antioxidant Strategies in Epilepsy: From Molecular Mechanisms to Threshold Management.International journal of molecular sciences · 2026Review
- Characterization of an isogenicInfection and immunity · 2026Article
- Article
- Infiltrating Monocyte Fate Switch in Retinal Degeneration: From Early Pathology to Late Homeostasis.Research square · 2026Article
- Advancing MSC-EV Therapies: Harnessing Preconditioning and Mito-EVs to Tackle Neuroinflammation and Neurodegeneration.Pharmaceutics · 2026Review
- Infiltrating monocytes augment alternative complement activation and exacerbate inherited retinal degeneration in a mouse model.Research square · 2026Article
- Review
- Exploring pathways leading to drug-resistant epilepsy for patients with cryptogenic new onset refractory status epilepticus.Epilepsia · 2026Article
- A model of new-onset refractory status epilepticus (NORSE) using intrahippocampal kainic acid in adolescent mice.Epilepsy research · 2026Article
- Live cell imaging of exogenous α-synuclein fibrils in primary microglia and neuron co-cultures.Biochemistry and biophysics reports · 2026Article
- Obstructive sleep apnea and seizures: pathophysiological mechanisms and clinical implications: a narrative review.Sleep & breathing = Schlaf & Atmung · 2026Review
- Circular RNA PTPN4 Contributes to Blood-Brain Barrier Disruption during Early Epileptogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Elucidating the putative role of cannabigerol: a hypothesis-generating review of neuroinflammatory and neuroprotective mechanisms with implications for drug-resistant epilepsy.Frontiers in pharmacology · 2026Review
- Red blood cell transfusion exacerbates phlebotomy-induced anemia-associated neuroinflammation in murine neonates.Transfusion · 2026Article
- Role of Glycerophospholipid Metabolism in Epilepsy.Current neuropharmacology · 2026Review
- The Potential of Coenzyme Q10 in Alzheimer's Disease: Reducing IL-17 Induced Inflammation and Oxidative Stress for Neuroprotection.Current drug research reviews · 2026Review
164 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
The generalized seizures of status epilepticus (SE) trigger a series of molecular and cellular events that produce cognitive deficits and can culminate in the development of epilepsy. Known early events include opening of the blood-brain barrier (BBB) and astrocytosis accompanied by activation of brain microglia. Whereas circulating monocytes do not infiltrate the healthy CNS, monocytes can enter the brain in response to injury and contribute to the immune response. We examined the cellular components of innate immune inflammation in the days following SE by discriminating microglia vs. brain-infiltrating monocytes. Chemokine receptor 2 (CCR2(+)) monocytes invade the hippocampus between 1 and 3 d after SE. In contrast, only an occasional CD3(+) T lymphocyte was encountered 3 d after SE. The initial cellular sources of the chemokine CCL2, a ligand for CCR2, included perivascular macrophages and microglia. The induction of the proinflammatory cytokine IL-1β was greater in FACS-isolated microglia than in brain-invading monocytes. However, Ccr2 knockout mice displayed greatly reduced monocyte recruitment into brain and reduced levels of the proinflammatory cytokine IL-1β in hippocampus after SE, which was explained by higher expression of the cytokine in circulating and brain monocytes in wild-type mice. Importantly, preventing monocyte recruitment accelerated weight regain, reduced BBB degradation, and attenuated neuronal damage. Our findings identify brain-infiltrating monocytes as a myeloid-cell subclass that contributes to neuroinflammation and morbidity after SE. Inhibiting brain invasion of CCR2(+) monocytes could represent a viable method for alleviating the deleterious consequences of SE.
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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.