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

1)内皮细胞（HUVECs）在细胞表面组成性表达Fas抗原。2)添加抗fas、CH-11.3诱导HUVECs凋亡)当HUVECs与中性粒细胞在抗fas存在下共培养时，它们相互失去粘附功能。4)抗fas处理中性粒细胞后，其细胞表面CD11b和CD18的表达降低。因此，粘附功能障碍依赖于中性粒细胞上的粘附分子。5)由于趋化因子和炎症细胞因子减少fas介导的HUVECs和中性粒细胞凋亡，这些药物维持了急性炎症组织中的中性粒细胞功能。6)相反，非甾体抗炎药增强fas介导的huvec和中性粒细胞的凋亡，这一事件可能是非甾体抗炎药抗炎功能的新策略。

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.