ArticleJournal of immunology (Baltimore, Md. : 1950)2018
S100A8/A9 Drives Neuroinflammatory Priming and Protects against Anxiety-like Behavior after Sepsis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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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Who cites it
43 citing papers in PubMed, 56 citations in OpenAlex.
- Restricted TCR Diversity and Expansion of CD177MedComm · 2026Article
- Glial cells in chronic inflammation: diversity, dysfunction and therapeutic targeting.Nature reviews. Immunology · 2026Review
- Blocking microglial reactivity via purinergic receptors prevents subacute cognitive deficits after TIA.EMBO molecular medicine · 2026Article
- Neuroimmune Mechanisms Transforming Acute Injury to Long-Term Brain Dysfunction After Sepsis.Clinics in chest medicine · 2026Review
- S100A8 aggravates sepsis-associated encephalopathy by promoting PFKFB3-dependent glycolysis and microglial neuroinflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Vascular-associated bacterial burden and neuroinflammatory transcriptional responses observed in models of pneumonic plague.Frontiers in microbiology · 2026Article
- Faecal inflammatory protein markers in children with autism spectrum disorder are comparable to their healthy siblings.Frontiers in psychiatry · 2026Article
- Targeting S100A8/A9: a molecular gateway to oral inflammation, microglial activation and neuroinflammation.Frontiers in immunology · 2026Review
- Spatial transcriptomics on an expanded dataset at the brain-electrode interface: exploration of variability and identification of novel biomarkers.Frontiers in neuroscience · 2026Article
- Mechanism of action and therapeutic potential of S100A8/A9 in neuroinflammation and cognitive impairment: From molecular target to clinical application (Review).International journal of molecular medicine · 2025Review
- Transcriptomic profile of microglia following inflammation-sensitized hypoxic-ischemic brain injury in neonatal rats suggests strong contribution to neutrophil chemotaxis and activation.Journal of neuroinflammation · 2025Article
- Targeting glial fibrillary acidic protein in glaucoma: a monoclonal antibody approach to modulate glial reactivity and neuroinflammation for neuroprotection.Journal of neuroinflammation · 2025Article
- Diverse NKT cells regulate early inflammation and neurological outcomes after cardiac arrest and resuscitation.Science translational medicine · 2024Article
- Article
- Usp14 deficiency removes α-synuclein by regulating S100A8/A9 in Parkinson's disease.Cellular and molecular life sciences : CMLS · 2024Article
- Neuroinflammation generated by HIV-infected microglia promotes dysfunction and death of neurons in human brain organoids.PNAS nexus · 2024Article
- NMI Functions as Immuno-regulatory Molecule in Sepsis by Regulating Multiple Signaling Pathways.Inflammation · 2024Article
- Extracellular proteins as potential biomarkers in Sepsis-related cerebral injury.Frontiers in immunology · 2023Article
- Histidine-Rich Glycoprotein Suppresses the S100A8/A9-Mediated Organotropic Metastasis of Melanoma Cells.International journal of molecular sciences · 2022Article
- Serum S100A8/A9 concentrations are associated with neuropsychiatric involvement in systemic lupus erythematosus: a cross-sectional study.BMC rheumatology · 2022Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Sepsis commonly results in acute and chronic brain dysfunction, which dramatically increases the morbidity associated with this common disease. Chronic brain dysfunction in animal models of sepsis survival is linked to persistent neuroinflammation and expression of multiple cytokines. However, we have found previously that microglia predominantly upregulate the damage associated molecule S100A8/A9 after sepsis. In this article, we show that S100A8/A9 is increased in the brains of patients who died of sepsis and that S100A8 is expressed in astrocytes and myeloid cells. Using a mouse model of sepsis survival, we show that S100A8/A9 is persistently expressed in the brain after sepsis.
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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.