ArticleBiology2025
Hypoxia Supports LPS-Driven Tolerance and Functional Activation in BV-2 Microglial Cells.
Article in Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
The trial behind it
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Who cites it
6 citing papers in PubMed.
- LPS and β-Glucan Induce Differential Memory-like Inflammatory Responses with Enhanced Reactivity in Neonatal Neutrophils Compared to Adults.International journal of molecular sciences · 2026Article
- Review
- Article
- Gut-derived small extracellular vesicles support trained innate immune tolerance in murine microglial cells.Frontiers in immunology · 2026Article
- Structure matters: commensalFrontiers in cellular neuroscience · 2026Article
- High-Altitude Hypoxia Injury: Systemic Mechanisms and Intervention Strategies on Immune and Inflammatory Responses.Antioxidants (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundProlonged hypoxia contributes to irreversible organ damage, particularly in the brain and heart. While chronic hypoxia is harmful, mild short-term hypoxia can trigger protective mechanisms. This study investigates how such hypoxic conditions affect BV-2 tolerant microglial cells in vitro, focusing on inflammation, metabolism, and functional activity. Although in vitro models provide a controlled setting, our findings may offer insights into microglial behavior in vivo under similar conditions.
methodsWe used various molecular and biochemical techniques to assess the inflammatory state of BV-2 microglia under hypoxia, measuring glycolytic activity (via lactate production), and evaluating migratory and phagocytic capacities in vitro.
resultsHypoxic conditions induced a more tolerant, anti-inflammatory phenotype in BV-2 cells, with decreased pro-inflammatory mediators and reduced glycolytic activity, regulated by the MyD88/NF-κB p65 pathway. Tolerance supports increased migration and phagocytosis, but under hypoxic conditions, these effects were significantly declined compared to normoxic conditions, mediated through the ERK1/2 pathway.
conclusionsThese findings suggest that short-term hypoxia may regulate microglial behavior and restore homeostasis, with implications for neuroinflammatory conditions.
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Registered trials
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