Background
Neuroinflammation is a component of age-related neurodegenerative diseases and cognitive decline. Saturated (SFA) and monounsaturated (MUFA) fatty acids are bioactive molecules that may play different extrinsic and intrinsic roles in neuroinflammation, serving as exogenous ligands for cellular receptors, or endogenous components of cell structural, energetic and signaling pathways.
Goals
The goal of this study was to:
- Determine the fatty acyl profile of BV2 microglial cells before and after acute activation with lipopolysaccharide (LPS).
- Investigate the effect of SFA and MUFA pretreatment on the production of an invasive, neurotoxic phenotype in BV2 cells.
Summary of findings
Acute activation of BV2 microglia resulted in an increase in the relative content of SFA, and a relative decrease in the content of MUFA. The major stearoyl-CoA desaturase (SCD) isoform in BV2 cells, SCD2, was significantly down-regulated by LPS.Cells treated with SFA or MUFA showed increased levels of secreted IL6 and MMP9-mediated proteolytic activity. A small but significant induction of cell death was found when SH-SY5Y neuronal cells were treated with conditioned medium from BV2 cells pretreated with fatty acids.
The findings suggest differential intrinsic roles for SFA and MUFA in activated microglial cells, but similar extrinsic roles for these fatty acid species in inducing activation. Expansion of SFA is important during microglial cell activation, but either supplemental SFA or MUFA may contribute to chronic low-grade neuroinflammation. This new information is critical in helping to fight against the onslaught of neurodegenerative diseases affecting our aging population.
