Basic research about pathophysiology of encephalopathy with hemolytic uremic syndrome

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In this research, fundamental research on the pathophysiology of the acute encephalopathy (HUS encephalopathy) accompanying the hemolytic uremic syndrome (HUS) by Shiga toxin-producing enterohemorrhagic Escherichia coli infection is done using the blood-brain barrier model by the human cerebral endothelial cell.(1)Chemokine expression of IL-8,MCP-1, etc. in the skin cell in the human cerebral endothelial cell by Stx stimulus, and the influence which chemokine has on leukocyte adhesion/shift ability or Gb3 expression ability are considered.(2)This cell culture system considers participation of leukocyte adhesion/shift ability, Gb3 expression ability, and Stx using the anti-chemokine antibody of anti-IL-8 antibody and anti-MCP-1 antibody.(3)Stx considers the influence, which it has on transfer factor NF-kappa B that participates in chemokine expression. As the blood-brain barrier model in a preparation stage, the cultivation system of the human cerebral endothelial cell were established, and the rise of chemokine was checked for guiding chemokine, such as IL-8 in a Stx stimulus, and MCP-1, by measurement of culture solution.Chemokine is considering the influence which it has on leukocyte adhesion/shift ability or Gb3 expression ability also in the current fiscal year now.Moreover, total RNA was extracted from the cell cultivated by Stx stimulus, the northern blot method of IL-8 and MCP-1 was performed, and significant expression was checked.The experiment using the anti-chemokine antibody of anti-IL-8 antibody and anti-MCP-1 antibody is under continuation now.It is under examination also about the transfer factor NF-kappa B activation by Stx stimulus. Also in the current fiscal year, acquisition of the human cerebral endothelial cell, which is an original model, is difficult, and is negotiating with the related organization and the company.The significant experiment data to a research subject are not drawn yet in three years.