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

口腔严重感染的发病机制：凋亡中性粒细胞的吞噬过程分析

基本信息

批准号：
10671907
负责人：
IWASE Masayasu
金额：
$ 1.79万
依托单位：
Showa University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10671907/
关键词：
Apoptosis Neutrophil Fas Caspase Glutathione Chemotactic factor FLIP Adhesion molecule 急性炎症細胞接着分子

项目摘要

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.

1. Anti-Fas处理的中性粒细胞的细胞粘附减少，因为中性粒细胞在凋亡过程中粘附分子发生了改变； CD11b、CD11c和CD18增强，CD11a、CD15和CD62L减少，CD31无变化。粘附分子的表达受FMLP、C5a、PAF、LTB4和IL-8等趋化因子影响。趋化因子增强中性粒细胞凋亡，但Fas不表达。2。术后第 1 天的中性粒细胞延迟了 Fas 介导的细胞凋亡，并伴有 caspase-3 和 -8 活性的降低。血浆因子对手术引起的急性炎症也抑制中性粒细胞凋亡。与常驻中性粒细胞相比，急性炎症中的中性粒细胞表现出谷胱甘肽水平降低，但 Fas 和 FLIP 水平的表达没有改变。急性炎症时血浆中含有大量谷胱甘肽和促炎细胞因子。抗促炎细胞因子降低血浆对细胞凋亡的抑制作用。外源性谷胱甘肽和 NAC 还通过 caspase-8.3 上游抑制 Fas 介导的中性粒细胞凋亡。 DMSO或RA分化的HL-60细胞由于细胞质中谷胱甘肽和FLIP水平的降低以及细胞膜中Fas表达的增强而增强了Fas介导的细胞凋亡。