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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
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Corticosterone potentiates ochratoxin A-induced microglial activation
Anchana Chansawhang1, Sataporn Phochantachinda2, Piya Temviriyanukul3
1The Center for Veterinary Diagnosis, Faculty of Veterinary Science, Mahidol University, Salaya, Phutthamonthon, Nakhon Pathom 73170, Thailand.
Biomolecular Concepts
|April 19, 2022
Summary
Ochratoxin A (OTA) activates microglia, increasing neuroinflammation. Corticosterone amplifies this OTA-induced inflammation via mineralocorticoid receptors, potentially worsening neurodegeneration.
Area of Science:
- Neuroscience
- Toxicology
- Immunology
Background:
- Microglial activation in the central nervous system (CNS) is linked to brain damage and neurodegenerative diseases.
- Ochratoxin A (OTA), a food-borne mycotoxin, exhibits neurotoxicity.
- Corticosteroids modulate CNS physiological functions.
Purpose of the Study:
- To investigate Ochratoxin A's (OTA) effects on microglial activation.
- To determine how corticosteroids influence OTA-induced microglial neuroinflammation.
- To elucidate the mechanisms underlying these interactions.
Main Methods:
- Murine microglial cells (BV-2) were stimulated with OTA.
- Corticosterone pre-treatment was used to assess potentiation effects on OTA-induced inflammation.
- Expressions of pro-inflammatory mediators (TNF-α, IL-1β, IL-6, iNOS) and nitric oxide (NO) were measured.
- Mitogen-activated protein kinase (MAPK) phosphorylation was analyzed via western blotting.
Main Results:
- OTA significantly upregulated mRNA expression of IL-6, TNF-α, IL-1β, and iNOS.
- OTA elevated IL-6 and NO levels in microglial cells.
- Corticosterone pre-treatment enhanced OTA-induced neuroinflammation.
- This enhancement was mediated by a mineralocorticoid receptor (MR)-dependent mechanism, involving increased ERK and p38 MAPK phosphorylation.
Conclusions:
- Ochratoxin A directly activates microglia, driving a neuroinflammatory response.
- Corticosterone potentiates OTA-induced neuroinflammation through MR and MAPK signaling pathways.
- Low endogenous corticosterone levels may exacerbate OTA-induced neurodegeneration.
