Effect of Lipopolysaccharide Derived from Pantoea agglomerans on the Phagocytic Activity of Amyloid {beta} by Primary Murine Microglial Cells

Background/Aim: Monophosphoryl lipid A, lipopolysaccharide (LPS)-derived Toll-like receptor (TLR) 4 agonist, has been shown to be effective in the prevention of Alzheimer's disease (AD) by enhancing phagocytosis of amyloid β (Aβ) by brain microglia. Our recent study demonstrated that oral administration of LPS derived from Pantoea agglomerans (LPSp) activates peritoneal macrophages and enhances the phagocytic activity via TLR4 signaling pathway; however, the effect of LPSp on Aβ phagocytosis in microglia is still unknown. Materials and Methods: Primary microglial cells were isolated from adult mouse brain by enzymatic digestion, following myelin removal and magnetic separation of cluster of differentiation (CD) 11b. Phagocytic analysis of the primary microglia was measured by using HiLyte™ Fluor 488-conjugated Aβ_1-42. Results: Using our protocols, the average yield of isolated CD11b⁺ cells was around 2.2x10⁵ cells per brain. CD11b⁺CD45⁺CD39⁺ cells were defined here as microglia. The phagocytic activity of Aβ_1-42 by the isolated microglia was confirmed. LPSp (10 ng/ml) pre-treatment for 18 h significantly increased Aβ phagocytic activity. Conclusion: The enhancement of Aβ_1-42 phagocytosis by LPSp treatment in the primary mouse microglia was demonstrated for the first time.

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