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

1)抗Fas抗体、CH-11可诱导HUVECs凋亡;抗Fas抗体处理后，HUVECs与中性粒细胞失去粘附功能;抗Fas抗体处理后，中性粒细胞表面CD 11b、CD 18表达下降。5）由于趋化因子和炎性细胞因子减少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中性粒细胞的功能。6）相反，NSAID促进Fas介导的HUVECs和中性粒细胞凋亡，这一事件是NSAID抗炎作用的新策略。

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.