Background/aim: Recent studies reported that lipopolysaccharide (LPS) exhibits beneficial effects on prevention of immune-related diseases by activating macrophages. We previously demonstrated that pre-treatment with LPS derived from Pantoea agglomerans (LPSp) activated amyloid β (Aβ) phagocytosis in mouse primary microglia. In the present study, we further examined the promotory effect on phagocytosis of phagocytic particles in the C8-B4 microglia cell line.
Materials and methods: Phagocytic analysis of C8-B4 cells was evaluated using phagocytic particles (latex beads or HiLyte™ Fluor 488-conjugated Aβ1-42).
Results: The phagocytic activity of latex beads was dependent on the concentration of beads and incubation time. LPSp, at as low as 100 pg/ml, significantly increased phagocytosis against the beads. In the experiment of Aβ1-42 phagocytosis, LPSp significantly increased Aβ phagocytic activity.
Conclusion: LPSp treatment was confirmed to enhance Aβ1-42 phagocytosis by mouse microglia. It is suggested that the use of LPSp may be a potential promising candidate for the prevention of Alzheimer's disease.
Keywords: Lipopolysaccharide; Pantoea agglomerans; amyloid β; microglia; toll-like receptor.
Copyright© 2017, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.