敗血症では炎症と凝固のクロストーク、いわゆる免疫反応による凝固障害（Immunothrombosis）が注目されている。これらは細菌の体内での広がりを抑制するための生体反応と考えられているが、その生成過程で血管内皮と白血球がどのように相互作用しているか不明な点が多い。我々はImmunothrombosisの病態解明のためにTMの炎症時と非炎症時の発現量をフローサイトメトリーと免疫染色により確認し、さらに白血球と血管内皮細胞との結合実験系を確立した。
Immunothrombosis, the immune response of blood vessels caused by preventing the spread of bactearia, plays an important role in inflammation and coagulation for sepsis. Many researchers are going to investigate that coagulation factor, like APC and EPCR, binds to leukocyte, leading to immunothrombosis. We have indicated that leukocyte LFA-1 and Mac-1 integrins bind to the serine/threonine-rich domain of thrombomodulin (TM). In fact, integrin-TM interactions might be involved in the dynamic regulation of leukocyte adhesion with endothelial cells, or immunothrombosis. Based on the results, we indicated here how the coagulation factor, TM on endothelial cell, is associated with leukocyte binding. First, we confirmed that the TNF -alpha induced inflammatory response downregulates TM expression on endothelial cells. Moreover we showed that pheripheral blood mononuclear cells (PBMCs) bind to human umbilical vein endothelial cell(HUVEC) dependent upon integrin activation.
β2インテグリンとトロンボモジュリンの結合が炎症と凝固に与える影響
2019RP0069
(250.89KB)
