Function of Eosinophils from Eosinophilic pneumonia : Purification and Analysis of Tcell-derived eosinophil chemotactic factor
嗜酸性粒细胞肺炎中嗜酸性粒细胞的功能:T细胞来源的嗜酸性粒细胞趋化因子的纯化和分析
基本信息
- 批准号:11670584
- 负责人:
- 金额:$ 2.37万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:1999
- 资助国家:日本
- 起止时间:1999 至 2001
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Although we couldn't success the finding of structure of eosinophil chemotactic factor derived from T-cell, we could get an interesting result during this time. We assessed the expression of galectin-9 with immunostaining and in situ hybridization both in the lesion of angiolymphoid hyperplasia with eosinophilia, and peripheral blood eosinophils of eosinophilic patients (E-Eos) in comparison with those of normal volunteers (N-Eos). Regulation of expression of galectin-9 on eosinophils and the effect of galectin-9 on apoptosis of eosinophil were also evaluated. Many eosinophils infiltrating the site were positive for galectin-9. Surface and intracellular immunoreactive galectin-9 was more evident in E-Eos than N-Eos. When eosinophils were cultured with IL-5 in vitro, the surface galectin-9 expression of E-Eos was significantly, down-regulated, although that of N-Eos was not affected. Treatment of eosinophils with dexarnethasone or anti-Fas antibody significantly up-regulated the surface galectin-9 expression of E-Eos. In contrast, dexamethasone controversially down-regulated the surface galectin-9 of N-Eos, although anti-Fas antibody failed to affect on the surface galectin-9 expression. We also found that recombinant galectin-9 significantly suppressed apoptosis of E-Eos, whereas it apparently enhanced apoptosis of N-Eos. Furthermore, dexamethasone-induced apoptosis of N-Eos was significantly suppressed by galectin-9, whereas galectin-9 failed to induce significant change in dexamethasoneinduced apoptosis of E-Eos. In contrast, apoptosis induced by anti-Fas antibody in both N-Eos and E-Eos was enhanced by galectin-9. These findings suggested that galectin-9 was produced by eosinophils, and galectin-9 showed heterogeneous effects and kinetics to eosinophils, and this factor might be one of crucial factors in eosinophilic inflammation.
虽然我们没有成功地发现来源于t细胞的嗜酸性趋化因子的结构,但我们在这段时间里得到了一个有趣的结果。我们用免疫染色和原位杂交的方法评估了半凝集素-9在血管淋巴样增生伴嗜酸性粒细胞增多病变中的表达,以及嗜酸性粒细胞增多患者(E-Eos)与正常志愿者(N-Eos)外周血嗜酸性粒细胞的表达。研究了半凝集素-9对嗜酸性粒细胞表达的调控作用以及对嗜酸性粒细胞凋亡的影响。浸润部位的许多嗜酸性粒细胞半凝集素-9阳性。表面和细胞内免疫反应性半凝集素-9在E-Eos比N-Eos更明显。IL-5体外培养嗜酸性粒细胞时,E-Eos表面半凝集素-9的表达明显下调,但N-Eos的表达不受影响。地塞米松或抗fas抗体处理嗜酸性粒细胞可显著上调E-Eos表面半凝集素-9的表达。相反,地塞米松有争议地下调了N-Eos的表面半凝集素-9,尽管抗fas抗体没有影响表面半凝集素-9的表达。我们还发现重组半乳糖凝集素-9显著抑制E-Eos的凋亡,而明显促进N-Eos的凋亡。此外,半凝集素-9能显著抑制地塞米松诱导的N-Eos细胞凋亡,而半凝集素-9不能显著改变地塞米松诱导的E-Eos细胞凋亡。而半凝集素-9可增强抗fas抗体诱导的N-Eos和E-Eos细胞凋亡。这些结果表明,半凝集素-9是由嗜酸性粒细胞产生的,并且对嗜酸性粒细胞具有异质性作用和动力学,该因子可能是嗜酸性粒细胞炎症的关键因素之一。
项目成果
期刊论文数量(9)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Naoki Saita, Tohru Yamanaka, Masayuki Ando, Mitsuomi Hirashima: "Apoptotic response of eosinophils in chronic eosinophilic pneumonia"European Respiratory Journal. 197(2). 190-194 (2001)
Naoki Saita、Tohru Yamanaka、Masayuki Ando、Mitsuomi Hirashima:“慢性嗜酸性粒细胞肺炎中嗜酸性粒细胞的凋亡反应”欧洲呼吸杂志。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Naoki Saita: "Apoptotic response of eosinophils in chronic eosinophilic pneumenia"European Respiratory Journel. 197. 190-194 (2001)
Naoki Saita:“慢性嗜酸性粒细胞肺炎中嗜酸性粒细胞的凋亡反应”欧洲呼吸杂志。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Naoki Sata et al: "Apoptotic response of eosinophils in chronic eosinophilic preumonic"European Respiratory Journanl. (発表予定). (2001)
Naoki Sata 等人:“慢性嗜酸性粒细胞前期的嗜酸性粒细胞凋亡反应”,欧洲呼吸杂志(即将出版)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Naoki Saita: "Apoptotic response of eosinophils in chronic eosinophilic pnecnnoria"European Respiratory Journal. 197. 190-197 (2001)
Naoki Saita:“慢性嗜酸性粒细胞肺炎中嗜酸性粒细胞的凋亡反应”欧洲呼吸杂志。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Naoki Saita et al: "Spontaneous production of IL-5 and its heterogeneous effect on eosinophils in an adult T-cell leukemia Patients "Allergology International. 49・2. 167-171 (2000)
Naoki Saita 等人:“成人 T 细胞白血病患者中 IL-5 的自发产生及其对嗜酸性粒细胞的异质性影响”,Allergology International 49・2 (2000)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
数据更新时间:{{ journalArticles.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ monograph.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ sciAawards.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ conferencePapers.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ patent.updateTime }}
SAITA Naoki其他文献
SAITA Naoki的其他文献
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
相似国自然基金
Epac1/2通过蛋白酶体调控中性粒细胞NETosis和Apoptosis在急性肺损伤中的作用研究
- 批准号:LBY21H010001
- 批准年份:2020
- 资助金额:0.0 万元
- 项目类别:省市级项目
基于Apoptosis/Ferroptosis双重激活效应的天然产物AlbiziabiosideA的抗肿瘤作用机制研究及其结构改造
- 批准号:81703335
- 批准年份:2017
- 资助金额:20.0 万元
- 项目类别:青年科学基金项目
双肝移植后Apoptosis和pyroptosis在移植物萎缩差异中的作用和供受者免疫微环境变化研究
- 批准号:81670594
- 批准年份:2016
- 资助金额:58.0 万元
- 项目类别:面上项目
Serp-2 调控apoptosis和pyroptosis 对肝脏缺血再灌注损伤的保护作用研究
- 批准号:81470791
- 批准年份:2014
- 资助金额:73.0 万元
- 项目类别:面上项目
Apoptosis signal-regulating kinase 1是七氟烷抑制小胶质细胞活化的关键分子靶点?
- 批准号:81301123
- 批准年份:2013
- 资助金额:23.0 万元
- 项目类别:青年科学基金项目
APO-miR(multi-targeting apoptosis-regulatory miRNA)在前列腺癌中的表达和作用
- 批准号:81101529
- 批准年份:2011
- 资助金额:22.0 万元
- 项目类别:青年科学基金项目
放疗与细胞程序性死亡(APOPTOSIS)相关性及其应用研究
- 批准号:39500043
- 批准年份:1995
- 资助金额:9.0 万元
- 项目类别:青年科学基金项目
相似海外基金
Development of an apoptosis biosensor for monitoring of breast cancer
开发用于监测乳腺癌的细胞凋亡生物传感器
- 批准号:
10719415 - 财政年份:2023
- 资助金额:
$ 2.37万 - 项目类别:
Milk fat globule-EGF factor 8 and hepatocyte apoptosis-induced liver wound healing response
乳脂肪球-EGF因子8与肝细胞凋亡诱导的肝脏创面愈合反应
- 批准号:
10585802 - 财政年份:2023
- 资助金额:
$ 2.37万 - 项目类别:
Interrogating the Fgl2-FcγRIIB axis on CD8+ T cells: A novel mechanism mediating apoptosis of tumor-specific memory CD8+ T cells
询问 CD8 T 细胞上的 Fgl2-FcγRIIB 轴:介导肿瘤特异性记忆 CD8 T 细胞凋亡的新机制
- 批准号:
10605856 - 财政年份:2023
- 资助金额:
$ 2.37万 - 项目类别:
Novel targeted therapy for FGFR inhibitor-resistant urothelial cancer and apoptosis based therapy for urothelial cancer
FGFR抑制剂耐药性尿路上皮癌的新型靶向治疗和基于细胞凋亡的尿路上皮癌治疗
- 批准号:
23K08773 - 财政年份:2023
- 资助金额:
$ 2.37万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Mechanistic analysis of apoptosis induction by HDAC inhibitors in head and neck cancer
HDAC抑制剂诱导头颈癌凋亡的机制分析
- 批准号:
23K15866 - 财政年份:2023
- 资助金额:
$ 2.37万 - 项目类别:
Grant-in-Aid for Early-Career Scientists
Interrogating the Fgl2-FcgRIIB axis: A novel mechanism mediating apoptosis of tumor-specific memory CD8+ T cells
探究 Fgl2-FcgRIIB 轴:介导肿瘤特异性记忆 CD8 T 细胞凋亡的新机制
- 批准号:
10743485 - 财政年份:2023
- 资助金额:
$ 2.37万 - 项目类别:
Investigating the role of apoptosis-resistance and the tumor environment on development and maintenance of sacrococcygeal teratomas
研究细胞凋亡抗性和肿瘤环境对骶尾部畸胎瘤发生和维持的作用
- 批准号:
10749797 - 财政年份:2023
- 资助金额:
$ 2.37万 - 项目类别:
The effects of glucose on immune cell apoptosis and mitochondrial membrane potential and the analysis of its mechanism by which glucose might modulate the immune functions.
葡萄糖对免疫细胞凋亡和线粒体膜电位的影响及其调节免疫功能的机制分析。
- 批准号:
22K09076 - 财政年份:2022
- 资助金额:
$ 2.37万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
XAF1 IN P53 SIGNALING, APOPTOSIS AND TUMOR SUPPRESSION
P53 信号传导、细胞凋亡和肿瘤抑制中的 XAF1
- 批准号:
10583516 - 财政年份:2022
- 资助金额:
$ 2.37万 - 项目类别:
Role of Thioredoxin system in regulation of autophagy-apoptosis cross talk in neurons: Uncovering Novel Molecular Interactions.
硫氧还蛋白系统在神经元自噬-凋亡串扰调节中的作用:揭示新的分子相互作用。
- 批准号:
RGPIN-2019-05371 - 财政年份:2022
- 资助金额:
$ 2.37万 - 项目类别:
Discovery Grants Program - Individual