Pathogenic mechanism of oral severe infection: Analysis of phagocytic process for apoptotic neutrophils

1.抗Fas抗体处理的中性粒细胞在凋亡过程中粘附分子发生改变，细胞粘附减少，CD 11b、CD 11 c、CD 18增强，CD 11 a、CD 15、CD 62 L减少，CD 31无变化。趋化因子FMLP、C5 a、PAF、LTB 4、IL-8等均能影响粘附分子的表达。在不表达Fas的情况下，趋化因子可促进神经细胞凋亡。术后第1天中性粒细胞Fas介导的凋亡延迟，伴caspase-3和-8活性降低。血浆中药物诱导的急性炎症因子也抑制中性粒细胞的凋亡。急性炎症中性粒细胞谷胱甘肽水平降低，但不改变表达Fas和FLIP水平相比，居民中性粒细胞。急性炎症时血浆中含有大量的谷胱甘肽和促炎细胞因子。血浆中抗炎细胞因子对细胞凋亡的抑制作用减弱。外源性谷胱甘肽和NAC也通过caspase-8.3上游抑制Fas介导的中性粒细胞凋亡。DMSO或RA诱导HL-60细胞分化后，由于胞浆内谷胱甘肽和FLIP水平降低，细胞膜Fas表达增强，Fas介导的细胞凋亡增强。

1. Anti-Fas treated neutrophils were reduced cell attachment, because adhesion molecules of neutrophils were altered during apoptotic process; enhancement of CD11b, CD11c and CD18, reduction of CD11a, CD15 and CD62L, no change of CD31. The expression of adhesion molecules was affected by chemotactic factors such as FMLP, C5a, PAF, LTB4 and IL-8. Neutrophil apoptosis was enhanced by chemotactic factors without the expression of Fas.2. Neutrophils on post-operative surgery day 1 were delayed Fas-mediated apoptosis accompanied with reduction of caspase-3 and -8 activities. Plasma factors on surgical-induced acute inflammation also inhibited apoptosis of neutrophils. Neutrophils on acute inflammation exhibited reduction of glutathione levels, but not alter expression of Fas and FLIP levels compared with resident neutrophils. Plasma on acute inflammation contained lots of glutathione and proinflammatory cytokines. Anti-proinflammatory cytokine decreased in inhibitory effect of plasma on apoptosis. Exogenous glutathione and NAC were also inhibited Fas-mediated apoptosis of neutrophils via upstream of caspase-8.3. Differentiated HL-60 cells by DMSO or RA were enhanced Fas-mediated apoptosis because of reduction of glutathione and FLIP levels in cytoplasma and enhancement of expression of Fas in membrane.