Regulation of systemic inflammatory response syndrome by TNF-related apoptosis inducing ligand which affect neutrophils exclusion and its potential clinical application.

TNF相关凋亡诱导配体影响中性粒细胞排除的全身炎症反应综合征的调节及其潜在的临床应用。

• 批准号: 23591870
• 负责人: KAMOHARA hidenobu
• 金额: $ 3.33万
• 依托单位: Kumamoto University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23591870/
• 关键词: SIRS; TRAIL; TRAIL受容体; 好中球; ＴＮＦα; ＩＦＮγ; アポトーシス; 実験医学; 白血球; 細胞死; Leukocytes; 分子生物学; TRAIL receptor

We have been identified that neutrophils express TRAIL and TRAIL-R which were induced by IFNgamma and reduced by TNFalpha. Finally, TNFalpha induced the netrophils apoptosis and IFNgamma reduced. In the present study, leukocytes were isolated in peripheral blood and local exudates from post-operative drain in SIRS. The level of TRAIL, TRAIL-R1, and -R2 (death receptor) mRNA were significant higher and the level of TRAIL-R3 and -R4 (decoy receptor) mRNA were significant lower in leukocytes from exudates than leukocytes form peripheral blood. Up- or down-regulation of TRAIL receptor expression by TNFalpha or IFNgamma can affect the susceptibility of neutrophils to TRAIL. In local inflammatory field, neutophils are activated by high amount of cytokines and neutophils expressing TRAIL, -R1 and -R2 can transit to be apoptosis. TRAIL signaling pathway could potentially regulate the fate of tissue-infiltrating neutrophils during SIRS.

我们已经鉴定了中性粒细胞表达TRAIL和TRAIL-R，其由IFN γ诱导并由TNF α降低。最后，TNF α诱导中性粒细胞凋亡，IFN γ减少。在本研究中，白细胞分离外周血和局部渗出液从术后引流SIRS。与外周血白细胞相比，渗出液白细胞中TRAIL、TRAIL-R1和-R2（死亡受体）mRNA水平显著升高，TRAIL-R3和-R4（诱饵受体）mRNA水平显著降低。TNF α或IFN γ上调或下调TRAIL受体表达可影响中性粒细胞对TRAIL的敏感性。在局部炎症区，中性粒细胞被大量细胞因子激活，表达TRAIL、-R1和-R2的中性粒细胞可转变为凋亡细胞。TRAIL信号通路可能调节SIRS时组织浸润中性粒细胞的命运。

项目成果

Serum microRNA-21 is a novel biomarker in patients with esophageal squamous cell carcinoma

• DOI: 10.1002/jso.23064
• 发表时间: 2012-08-01
• 期刊: JOURNAL OF SURGICAL ONCOLOGY
• 影响因子: 2.5
• 作者: Kurashige, Junji;Kamohara, Hidenobu;Baba, Hideo
• 通讯作者: Baba, Hideo