ArticleJournal of cellular and molecular medicine2020
Characterization and modulation of microglial phenotypes in an animal model of severe sepsis.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 43 citations in OpenAlex.
- Associations Between Neuromuscular Fatigue, Anxiety, and Peripheral Biomarkers of Neuronal Injury, Inflammation, and Mitochondrial Dysfunction in Treatment-Naïve Relapsing-Remitting Multiple Sclerosis.Brain and behavior · 2026Article
- Current knowledge and challenges of sepsis-associated encephalopathy.Intensive care medicine · 2026Review
- INPP5D Upregulation by Minocycline Mitigates Sepsis-Associated Neuroinflammation and Neuronal Dysfunction Via Microglial Autophagy and Antioxidant Pathways.Inflammation · 2026Article
- Bloodstream Infection-induced Neuroinflammation: from Systemic Infection To Brain Invasion.Current microbiology · 2025Review
- Convergence of sepsis-associated encephalopathy pathogenesis onto microglia.Journal of translational medicine · 2025Review
- Single-nucleus transcriptomics reveals sepsis-related neurovascular dysfunction in the human hippocampus.Frontiers in immunology · 2025Article
- Lung-brain crosstalk: Behavioral disorders and neuroinflammation in septic survivor mice.Brain, behavior, & immunity - health · 2024Article
- Minocycline mitigates sepsis-induced neuroinflammation and promotes recovery in male mice: Insights into neuroprotection and inflammatory modulation.Physiological reports · 2024Article
- Microglial Activation: Key Players in Sepsis-Associated Encephalopathy.Brain sciences · 2023Review
- Article
- Diabetes Exacerbates Sepsis-Induced Neuroinflammation and Brain Mitochondrial Dysfunction.Inflammation · 2022Article
- Reactive Microgliosis in Sepsis-Associated and Acute Hepatic Encephalopathies: An Ultrastructural Study.International journal of molecular sciences · 2022Article
- Constitutively active microglial populations limit anorexia induced by the food contaminant deoxynivalenol.Journal of neuroinflammation · 2022Article
- Mitochondrial protective effects caused by the administration of mefenamic acid in sepsis.Journal of neuroinflammation · 2022Article
- Pre-treatment and continuous administration of simvastatin during sepsis improve metabolic parameters and prevent CNS injuries in survivor rats.Molecular and cellular biochemistry · 2022Article
- Article
- Iron dyshomeostasis and time-course changes in iron-uptake systems and ferritin level in relation to pro-inflammatory microglia polarization in sepsis-induced encephalopathy.Frontiers in physiology · 2022Article
- Oxytocin and Related Peptide Hormones: Candidate Anti-Inflammatory Therapy in Early Stages of Sepsis.Frontiers in immunology · 2022Review
- Sinomenine activation of Nrf2 signaling prevents inflammation and cerebral injury in a mouse model of ischemic stroke.Experimental and therapeutic medicine · 2021Article
- The Protective Effect of PK-11195 on Cognitive Impairment in Rats Survived of Polymicrobial Sepsis.Molecular neurobiology · 2021Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We aim to characterize the kinetics of early and late microglial phenotypes after systemic inflammation in an animal model of severe sepsis and the effects of minocycline on these phenotypes. Rats were subjected to CLP, and some animals were treated with minocycline (10 ug/kg) by i.c.v. administration. Animals were killed 24 hours, 5, 10 and 30 days after sepsis induction, and serum and hippocampus were collected for subsequent analyses. Real-time PCR was performed for M1 and M2 markers. TNF-α, IL-1β, IL-6, IL-10, CCL-22 and nitrite/nitrate levels were measured. Immunofluorescence for IBA-1, CD11b and arginase was also performed. We demonstrated that early after sepsis, there was a preponderant up-regulation of M1 markers, and this was not switched to M2 phenotype markers later on. We found that up-regulation of both M1 and M2 markers co-existed up to 30 days after sepsis induction. In addition, minocycline induced a down-regulation, predominantly, of M1 markers. Our results suggest early activation of M1 microglia that is followed by an overlap of both M1 and M2 phenotypes and that the beneficial effects of minocycline on sepsis-associated brain dysfunction may be related to its effects predominantly on the M1 phenotype.
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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.