Yutaro Kobayashi1, Hiroyuki Inagawa2,3,4, Chie Kohchi2,5, Katsuichiro Okazaki6, Ran Zhang3, Hideki Kobara7, Tsutomu Masaki7, Gen-Ichiro Soma2,3,4. 1. Department of Integrated and Holistic Immunology, Faculty of Medicine, Kagawa University, Kagawa, Japan kobayashi@shizenmeneki.org. 2. Department of Integrated and Holistic Immunology, Faculty of Medicine, Kagawa University, Kagawa, Japan. 3. Control of Innate Immunity, Technology Research Association, Kagawa, Japan. 4. Research Institute for Healthy Living, Niigata University of Pharmacy and Applied Life Sciences, Niigata, Japan. 5. Macrophi Inc., Takamatsu, Kagawa, Japan. 6. Department of Applied Biological Science, Faculty of Agriculture, Kagawa University, Kagawa, Japan. 7. Department of Gastroenterology and Neurology, Faculty of Medicine, Kagawa University, Kagawa, Japan.
Abstract
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. Copyright
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. Copyright