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Published on: October 31, 2017
Exposure to the saturated free fatty acid palmitate alters BV-2 microglia inflammatory response
Linda M Tracy1, Filip Bergqvist, Elena V Ivanova
1Department of Neurochemistry, Stockholm University, SE-106 92, Stockholm, Sweden.
Abstract:
Elevated levels of free fatty acids (FFAs) in plasma and increased incidence of chronic systemic inflammation are associated with obesity. In the brain, activated microglia are believed to play different roles during inflammation that may either be neuroprotective or promote neurodegeneration. Here, we have investigated the effects of FFAs on microglial response to inflammatory stimuli. Our results indicate that the saturated FFA palmitate on its own induces alternative activation of BV-2 microglia cells. Further, pre-exposure to palmitate changed the response of microglia to lipopolysaccharide (LPS). We show that palmitate affects the mRNA levels of the pro-inflammatory cytokines interleukin-1β and interleukin-6. The transcription factor CCAAT/enhancer-binding protein δ is also affected by pre-exposure to palmitate. Furthermore, the phagocytic activity of microglia was investigated using fluorescent beads. By analyzing the bead uptake by fluorescence-activated cell sorting, we found that palmitate alone, as well as together with LPS, stimulated the phagocytic activity of microglia. Taken together, our results suggest that exposure of microglia to increased levels of free fatty acids may alter the consequences of classical inflammatory stimuli.
Insights
Elevated free fatty acids (FFAs) alter microglial cell responses to inflammation. Palmitate, a saturated FFA, alone or with LPS, enhances microglial phagocytic activity and affects inflammatory gene expression.
Area of Science:
- Neuroscience
- Immunology
- Metabolic Research
Background:
- Obesity is linked to elevated plasma free fatty acids (FFAs) and chronic systemic inflammation.
- Microglia, the brain's immune cells, have dual roles in neuroinflammation, potentially being neuroprotective or promoting neurodegeneration.
- Understanding how FFAs influence microglial inflammatory responses is crucial for neurodegenerative disease research.
Purpose of the Study:
- To investigate the impact of FFAs on microglial activation and response to inflammatory stimuli.
- To determine how palmitate, a saturated FFA, affects microglial cells.
- To elucidate the mechanisms underlying FFA-mediated modulation of neuroinflammation.
Main Methods:
- Utilized BV-2 microglia cell line for experiments.
- Assessed microglial activation and inflammatory marker expression.
- Quantified phagocytic activity using fluorescent beads and fluorescence-activated cell sorting.
- Analyzed mRNA levels of key inflammatory mediators and transcription factors.
Main Results:
- Palmitate alone induced alternative activation in BV-2 microglia cells.
- Pre-exposure to palmitate altered microglial responses to lipopolysaccharide (LPS).
- Palmitate modulated mRNA levels of interleukin-1β, interleukin-6, and CCAAT/enhancer-binding protein δ.
- Palmitate, with or without LPS, significantly stimulated microglial phagocytic activity.
Conclusions:
- Increased FFAs can modify microglial responses to classical inflammatory signals.
- Palmitate exposure influences microglial activation state, inflammatory gene expression, and phagocytosis.
- These findings suggest a potential mechanism by which metabolic alterations in obesity may impact brain inflammation and neurodegeneration.
