热休克蛋白70通过上调肠道γδ T细胞的Th17反应来保护小鼠免受感染后肠易激综合征的影响。
Heat shock protein 70 protects mouse against post-infection irritable bowel syndrome via up-regulating intestinal γδ T cell's Th17 response.
作者信息
He Zhoutao, Sun Xiaoning, Ma Zhichao, Fu Jiao, Huang Baili, Liu Fujin, Chen Yi, Deng Taozhi, Han Xiangyang, Sun Deming, Lan Cheng
机构信息
1Department of Gastroenterology, Hainan General Hospital, Xiu Hua Road 19th, Xiu Ying District, Haikou, 570311 Hainan Province China.
2Medical Research Center, Hainan General Hospital, Haikou, 570311 Hainan Province China.
出版信息
Cell Biosci. 2018 Jun 5;8:38. doi: 10.1186/s13578-018-0237-z. eCollection 2018.
BACKGROUND
This study investigated the role of HSP70 in modulating intestinal γδ T cells' Th17 response in -induced PI-IBS mice model.
METHODS
The intestinal HSP70's expression and mRNA level were measured by Western blot and RT-PCR. The intestinal γδ T cell's morphological changes were analyzed using immunofluorescence staining and confocal laser scanning microscope. The pro-inflammatory cytokines' level was detected by ELISA. The isolated and purified γδ T cells were pre-incubated with HSP70 and their functions including proliferation, apoptosis, activation and production of IL-17 were also detected.
RESULTS
Heat treatment augmented intestinal HSP70 expression and alleviated the clinical presentations in PI-IBS mice. Meanwhile, intestinal γδ T cells and local IL-17 level were increased by pre-induction of HSP70. HSP70 promoted the proliferation of PI-IBS mice's intestinal γδ T cells, inhibited the apoptosis and stimulated these cells to secret IL-17 rather than IFN-γ.
CONCLUSION
Our results suggest that HSP70 plays a protective role via up-regulating intestinal γδ T cell's Th17 response in PI-IBS mice.
背景
本研究调查了热休克蛋白70（HSP70）在调节诱导性肠易激综合征（PI-IBS）小鼠模型中肠道γδ T细胞的Th17反应中的作用。
方法
采用蛋白质免疫印迹法（Western blot）和逆转录聚合酶链反应（RT-PCR）检测肠道HSP70的表达及mRNA水平。运用免疫荧光染色和共聚焦激光扫描显微镜分析肠道γδ T细胞的形态变化。通过酶联免疫吸附测定（ELISA）检测促炎细胞因子水平。将分离纯化的γδ T细胞与HSP70预孵育，并检测其增殖、凋亡、活化及白细胞介素-17（IL-17）产生等功能。
结果
热处理增强了PI-IBS小鼠肠道HSP70的表达，并减轻了其临床表现。同时，预先诱导HSP70可使肠道γδ T细胞及局部IL-17水平升高。HSP70促进了PI-IBS小鼠肠道γδ T细胞的增殖，抑制了其凋亡，并刺激这些细胞分泌IL-17而非干扰素-γ（IFN-γ）。
结论
我们的结果表明，HSP70通过上调PI-IBS小鼠肠道γδ T细胞的Th17反应发挥保护作用。
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