Qingchang Huashi granule ameliorates experimental colitis via restoring the dendritic cell-mediated Th17/Treg balance.

Qingchang Huashi granule ameliorates experimental colitis via restoring the dendritic cell-mediated Th17/Treg balance.
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清肠化湿颗粒通过恢复树突状细胞介导的Th17Treg平衡改善实验性结肠炎

DOI:
10.1186/s12906-020-03088-y
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发表时间:
2020-09-23
影响因子:
3.9
通讯作者:
Feng W
Feng W
中科院分区:
医学3区
文献类型:
--
作者:
Jia J;Zheng K;Shen H;Yu J;Zhu P;Yan S;Xu Y;Zhu L;Lu Y;Gu P;Feng W

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辅助性T细胞17(Th 17)和调节性T细胞(Tcl 4)之间的平衡参与免疫耐受。树突状细胞(DC)介导的T细胞破坏免疫耐受参与溃疡性结肠炎(UC)的发病机制。清肠化湿颗粒治疗UC的作用已被证实与抑制DC的活化有关。本研究的目的是探讨QCHS通过调节DC在治疗UC中恢复Th 17/Treg平衡的机制。采用2,4,6-三硝基苯磺酸(TNBS)诱导的实验性结肠炎模型,观察QCHS对Th 17细胞、TCFs和DC的影响。此外,我们将QCHS处理的DC注射到结肠炎模型中以测试QCHS是否通过DC调节Th 17/Treg平衡。通过流式细胞仪(FACS)分析Th 17和Th 17细胞。通过ELISA、Western印迹和qRT-PCR测量IL-10、IL-17和Foxp 3。在结肠炎小鼠中,QCHS和QCHS处理的DC均改善结肠组织病理学,减少Th 17细胞分化并抑制IL-17产生,同时促进CD 4 + CD 25 + Foxp 3 + Treg分化并增加IL-10和Foxp 3表达。此外,QCHS降低DC上的CD 86和MHC-II表达,降低离体IL-12产生,并恢复结肠炎模型中的Th 17/Treg比率。这项研究的结果表明,QCHS通过恢复DC介导的Th 17/Treg平衡来改善TNBS诱导的结肠炎。
The balance between T helper 17 (Th17) cells and regulatory T cells (Tregs) is involved in immunological tolerance. Destruction of immunological tolerance by dendritic cell (DC)-mediated T cells is involved in the pathogenesis of ulcerative colitis (UC). Qingchang Huashi granule (QCHS) has been confirmed in the treatment of UC involved by inhibiting the activation of DCs. The aim of this study was to investigate the mechanism through which QCHS restores the Th17/Treg balance by modulating DCs in the treatment of UC. The effects of QCHS on Th17 cells, Tregs and DCs were detected in a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced experimental colitis model. Furthermore, we injected QCHS-treated DCs into colitis model to test whether QCHS modulates the Th17/Treg balance via DCs. Tregs and Th17 cells were analyzed by FACS. IL-10, IL-17, and Foxp3 were measured by ELISA, Western blot and qRT-PCR. Both QCHS and QCHS-treated DCs improved colonic histopathology, diminished Th17 cell differentiation and inhibited IL-17 production while promoting CD4+CD25+Foxp3+ Treg differentiation and augmenting IL-10 and Foxp3 expression in colitis mice. Additionally, QCHS reduced CD86 and MHC-II expression on DCs, decreased IL-12 production ex vivo and restored the Th17/Treg ratio in the colitis model. The findings of this study indicate that QCHS ameliorates TNBS-induced colitis by restoring the DC-mediated Th17/Treg balance.
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