ArticleJournal of immunology (Baltimore, Md. : 1950)2019
Long-Term Microgliosis Driven by Acute Systemic Inflammation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- The Key Drivers of Brain Injury by Systemic Inflammatory Responses after Sepsis: Microglia and Neuroinflammation.Molecular neurobiology · 2023Pooled it
- Bacterial extracellular vesicles indirectly destabilize a human stem cell-derived blood-brain barrier on-chip through pro-inflammatory stimulation of immune cells.Lab on a chip · 2026Article
- Microglia in systemic neuroimmune communication: functions beyond phagocytosis.Trends in immunology · 2026Review
- Antibiotics modulate Escherichia coli-derived bacterial extracellular vesicle production and their upregulation of ICAM-1 in human endothelial cells.Biology open · 2026Article
- Bacterial extracellular vesicles indirectly destabilize a human stem cell-derived blood-brain barrier on-chip through pro-inflammatory stimulation of immune cells.bioRxiv : the preprint server for biology · 2026Article
- Convergence of sepsis-associated encephalopathy pathogenesis onto microglia.Journal of translational medicine · 2025Review
- Transcript and Lipid Profile Alterations in Astrocyte-Neuron Mitochondrial Transfer Under Lipopolysaccharide Exposure: An In Vitro Study.Journal of neurochemistry · 2025Article
- Identification and Evaluation of Lipocalin-2 in Sepsis-Associated Encephalopathy via Machine Learning Approaches.Journal of inflammation research · 2025Article
- Hybrid Amyloid Quantum Dot Nano-Bio Assemblies to Probe Neuroinflammatory Damage.ACS chemical neuroscience · 2024Article
- Plac8-ERK pathway modulation of monocyte function in sepsis.Cell death discovery · 2024Article
- Targeted rescue of synaptic plasticity improves cognitive decline in sepsis-associated encephalopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Infectious Diseases.Advances in neurobiology · 2024Review
- Pericytes Enrich the Basement Membrane and Reduce Neutrophil Transmigration in an In Vitro Model of Peripheral Inflammation at the Blood-Brain Barrier.Biomaterials research · 2024Article
- Long non-coding RNA small nucleolar RNA host gene 8 (SNHG8) sponges miR-34b-5p to prevent sepsis-induced cardiac dysfunction and inflammation and serves as a diagnostic biomarker.Archives of medical science : AMS · 2024Article
- Determinants of urinary tract infection in hospitalized patients with acute ischemic stroke.BMC neurology · 2023Article
- Prior exposure to stress exacerbates neuroinflammation and causes long-term behavior changes in sepsis.Heliyon · 2023Article
- Microglia mediate neurocognitive deficits by eliminating C1q-tagged synapses in sepsis-associated encephalopathy.Science advances · 2023Article
- Role of microglia in HIV-1 infection.AIDS research and therapy · 2023Review
- Progressive cognitive impairment after recovery from neuroinvasive and non-neuroinvasiveFrontiers in immunology · 2023Article
- Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Severe sepsis, a systemic inflammatory response to infection, is an increasing cause of morbidity in intensive care units. During sepsis, the vasculature is profoundly altered, leading to release of microbial virulence factors and proinflammatory mediators to surrounding tissue, causing severe systemic inflammatory responses and hypoxic injury of multiple organs. To date, multiple studies have explored pathologic conditions in many vital organs, including lungs, liver, and kidneys. Although data suggest that sepsis is emerging as a key driver of chronic brain dysfunction, the immunological consequence of severe inflammatory responses in the brain remain poorly understood. In this study, we used C57BL/6 sepsis mouse models to establish a disease phenotype in which septic mice with various degrees of severity recover. In the early phases of sepsis, monocytes infiltrate the brain with significantly elevated proinflammatory cytokine levels. In recovered animals, monocytes return to vehicle levels, but the number of brain-resident microglia is significantly increased in the cortex, the majority of which remain activated. The increase in microglia number is mainly due to self-proliferation, which is completely abolished in CCR2 knockout mice. Collectively our data suggest that early monocyte infiltration causes permanent changes to microglia during sepsis, which may ultimately dictate the outcome of future infections and neuropathological diseases.
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What OpenQuestion holds
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.