We can’t show the full text here under this license. Use the link below to read it at the source.
Inflammatory factors and amyloid β-induced microglial polarization promote inflammatory crosstalk with astrocytes
Inflammation and amyloid beta cause immune cells in the brain to trigger inflammation with support cells
AI simplified
Abstract
M1 microglial medium increased astrocyte production of pro-inflammatory factors, while M2 microglial medium enhanced anti-inflammatory factors.
- Microglial polarization may alter immune interactions between microglia and astrocytes in Alzheimer's disease.
- M1 microglia are associated with the secretion of pro-inflammatory factors such as interleukin-1β, tumor necrosis factor α, and interleukin-6.
- M2 microglia are linked to the production of anti-inflammatory factors including interleukin-4 and interleukin-10.
- Exposure to amyloid-β alone or with inflammatory substances may induce pro-inflammatory activity in both M1 microglia and astrocytes.
- Nuclear factor κB p65 was upregulated in pro-inflammatory microglia and astrocytes, suggesting a role in inflammation.
- Stat6 was upregulated in M2 microglia and anti-inflammatory astrocytes, indicating a potential mechanism for regulating inflammation.
AI simplified