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Hypoxia supports LPS-driven tolerance and functional activation in BV-2 microglial cells

Background: Prolonged 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...

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Main Authors: Chavero Vargas, Alicia (Author) , Köstlin-Gille, Natascha (Author) , Bauer, Reinhard (Author) , Dietz-Ziegler, Stefanie (Author) , Lokaj, Anita S. (Author) , Lutterbach, Soumya (Author) , Gille, Christian (Author) , Lajqi, Trim (Author)
Format: Article (Journal)
Language:English
Published: 28 October 2025
In: Biology
Year: 2025, Volume: 14, Issue: 11, Pages: 1-23
ISSN:2079-7737
DOI:10.3390/biology14111512
Online Access:Verlag, kostenfrei, Volltext: https://doi.org/10.3390/biology14111512
Verlag, kostenfrei, Volltext: https://www.mdpi.com/2079-7737/14/11/1512
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Author Notes:Alicia Chavero Vargas, Natascha Köstlin-Gille, Reinhard Bauer, Stefanie Dietz-Ziegler, Anita S. Lokaj, Soumya Lutterbach, Christian Gille and Trim Lajqi
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Summary:Background: Prolonged 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. Methods: We 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. Results: Hypoxic 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. Conclusions: These findings suggest that short-term hypoxia may regulate microglial behavior and restore homeostasis, with implications for neuroinflammatory conditions.
Item Description:Veröffentlicht: 28. Oktober 2025
Gesehen am 27.01.2026
Physical Description:Online Resource
ISSN:2079-7737
DOI:10.3390/biology14111512

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