Yeonseung Han
Yonsei University, Korea
Title: Activated M2 phenotype microglia induce differentiation and polarization of monocyte and chemo-attraction in in vitro system
Biography
Biography: Yeonseung Han
Abstract
The inflammatory response following acute ischemic stroke is a well-known and widely studied phenomenon. However, the mechanism of neuro-inflammation is still unknown. Microglia and monocyte are now recognized to play a major role in neuro-inflammation after ischemic stroke. Microglia are the resident macrophages of brain. Macrophages originated from monocyte also have a highly phagocytic capacity after ischemic stroke. In this study, we explored the activated microglia by ischemic stroke affect to differentiation of monocyte. BV-2 cells (microglia cell line) were treated with lipopolysaccharides (LPS; 10ng/mL) for polarization to M1 phenotype and treated with interleukin-4 (IL-4; 20ng/mL) for polarization to M2 phenotype. After BV2 cells were activated with LPS and IL-4 for 1 d, cells were washed and M1 and M2 phenotype conditioned media were harvested at 3 d. THP-1 cells (monocyte cell line) were cultured in M1 and M2 phenotype conditioned media of BV2 cells. THP-1 cells were also treated with each following substances; IL-10, IL-1 beta, TGF-alpha and TGF-beta. It is well known that CD11b positive cells consider as M0 macrophage, CD86 positive cells as M1 macrophage and CD206 positive cells as M2 macrophage. THP-1 cells treated with M2 phenotype conditioned media expressed CD206 immunoreactivity in condition with and without phorbol-12-myristate-13-acetate (PMA; 10ng/mL). And, CD11b immunopositive cells were significantly high in the IL-1 beta and TGF-beta treated group. CD206 positive cells were also highly observed in the TGF-beta treated group but less than M2 phenotype conditioned media treated group. Our data supports that the cytokine secreted from M2 phenotype microglia might induce differentiation of monocyte into M2 phenotype macrophage in in vitro system.
