MECHANISM OF PROLONGED INFLAMMATION IN THE ORAL:EFFECT OF NEUTROPHIL APOPTOSIS ON ENDOTHELIAI CELLS

点击翻译按钮获取中文摘要

1) Endothelial cells, HUVECs, constitutively expressed Fas antigen on cell surface.2) HUVECs were induced apoptosis by the addition of anti-Fas, CH-11.3) When HUVECs and neutrophils were co cultured in the presence of anti-Fas, they lost adhesive function each other.4) When neutrophils were treated with anti-Fas, the expressions of CD11b and CD18 decreased in its cell surface. Therefore, adhesive dysfunction was dependent on adhesive molecule on neutrophils.5) Because chemokine and inflammatory cytokine reduced Fas-mediated apoptosis on HUVECs and neutrophils, these agents maintained neutrophil function in the acute inflammatory tissues.6) In contrast, NSAIDs enhanced Fas-mediated apoptosis on HUVECs and neutrophils, then this event was new a strategy for anti-infiammatory function of NSAIDs.