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Attenuation of butyric acid-induced T cell apoptosis by human gingival fibroblast

人牙龈成纤维细胞减弱丁酸诱导的 T 细胞凋亡

基本信息

批准号：
11671818
负责人：
OCHIAI Tamoko
金额：
$ 1.98万
依托单位：
Nihon University
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 2000
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11671818/
关键词：
APOPTOSIS T CELLS FIBR OBLAST BUTYRIC ACID INFLAMMATORY CYTOKINES CD44 CD47 CD58 揮発性脂肪酸歯肉

项目摘要

(1) Although butyric acid exhibited a dose-dependent inhibition in F41-G and Ca 9-22 cells, their effect was not prominent compared to the data with T-, B- and monocytic cells. Furthermore, the results of DNA fragmentation assay indicated that butyric acid did not induced apoptosis in human gingival fibroblasts (Gin 1, F41G and H.pulp).(2) When the culture supernatants of gingival fibroblasts were assayed for IL-1α, IL-1β, IL-6, IL-8, IL-11, TNF α and TGF β by use of ELISA kits, butyric acid significautly increased IL-6, IL-8 and IL-11 production. Maximum levels of these cytokines were noted by the addition of 5 mM butyric acid in Gin 1, F41-G and H.pulp cells. These levels were 1,500 to 1,900 pg/ml (IL-6), ca.4,000 to 5,000 pg/ml (IL-8), and ca.900 to 1,100 pg/ml (IL-11).(3) Co-culturing Jurkat cells with F41G or Gin 1 cells using intercup partially rescued butyric acid- or Fas-induced Jurkat cell apoptosis, suggest a role for a soluble factor released from fibroblasts in preventing T cell-apoptosis.(4) IL-6 and IL-8 slightly stimulated butyric acid- or Fas-induced Jurkat cell apoptosis in a dose-dependent manner, in contrast, IL-11 significantly suppressed these Jurkat cell apoptosis dose-dependently. These results suggest that the sum of their effects of the inflammatory cytokines such as IL-6, IL-8 and IL-11, produced in fibroblast by the addition of butyric acid, are concernted in the attenuation of T cell apoptosis by gingival fibroblast.(5) Furthemore, the direct cell-cell interaction indicated that the apoptosis of Jurkat T cells attached on the gingival fibroblasts was significantly rescued. CD47, CD44 and CD58 expression on the fibroblasts was increased by the addition of butyric acid, suggest that the increase of these cell surface molecule was concerned with the suppression of T cell apoptosis induced by butyric acid.

(1)虽然丁酸在F41-G和Ca 9-22细胞中表现出剂量依赖性抑制，但与T细胞、B细胞和单核细胞的数据相比，其作用并不显著。DNA片段化分析结果表明丁酸对人牙龈成纤维细胞（Gin 1、F41 G和H.pulp）无诱导凋亡作用。(2)用ELISA试剂盒检测牙龈成纤维细胞培养上清中IL-1α、IL-1β、IL-6、IL-8、IL-11、TNF α和TGF β的含量，丁酸能显著增加IL-6、IL-8和IL-11的产生。通过在Gln 1、F41-G和H.牙髓细胞中加入5 mM丁酸，观察到这些细胞因子的最大水平。这些水平为1，500至1，900 pg/ml（IL-6）、约4，000至5，000 pg/ml（IL-8）和约900至1，100 pg/ml（IL-11）。(3)共培养Jurkat细胞与F41 G或Gin 1细胞使用intercup部分拯救丁酸或Fas诱导的Jurkat细胞凋亡，表明从成纤维细胞释放的可溶性因子在防止T细胞凋亡中的作用。(4)IL-6和IL-8以剂量依赖方式轻微刺激丁酸或Fas诱导的Jurkat细胞凋亡，而IL-11则以剂量依赖方式显著抑制这些Jurkat细胞凋亡。这些结果表明，丁酸在牙龈成纤维细胞中产生的炎性细胞因子如IL-6、IL-8和IL-11的作用的总和与牙龈成纤维细胞减弱T细胞凋亡有关。(5)此外，直接的细胞-细胞相互作用表明，牙龈成纤维细胞上的Jurkat T细胞的凋亡显着拯救。丁酸诱导成纤维细胞表面分子CD 47、CD 44和CD 58表达增加，提示这些细胞表面分子的增加与丁酸抑制T细胞凋亡有关。