THE ACUTE EFFECTS OF β-FUNALTREXAMINE ON LIPOPOLYSACCHARIDE-INDUCED INFLAMMATION IN BV2 MURINE MICROGLIAL CELLS

Inflammation is a crucial and driving factor in many pathological conditions. Additionally, neuroinflammation has been associated with poorer outcomes in brain and spinal cord injuries, as well as fueling and exacerbating neurodegenerative and neuropsychiatric conditions. Microglia are keystones of neuroinflammation, but efforts to isolate their role in neuroinflammation have been challenging due to heterogeneity based on brain region, sex, age, and/or disease. There is a dearth of pharmaceuticals that can cross the blood-brain barrier to target neuroinflammation without dependency or toxicity issues. Our lab has been investigating the impact of a well-tolerated, non-addictive irreversible μ-opioid antagonist and reversible kappa-opioid agonist, β-funaltrexamine (β-FNA), on neuroinflammation, peripheral inflammation, and inflammation-induced behavior deficits. Previously, our lab discovered that β-FNA has anti-inflammatory effects on normal human astrocytes and male C57BL/6J mice, as well as ameliorating effects on anxiety-like and sickness-like behavior in male C57BL/6J mice. Now, we examined the effects of acute β-FNA treatment on lipopolysaccharide (LPS)-stimulated BV2 murine microglial cells. We discovered that β-FNA dampens morphological changes associated with LPS-driven microglial activation and inhibits CCL2. Consequently, these findings provide novel insights into the cell-specific anti-inflammatory effects of β-FNA and its potential as a therapeutic agent.