Paeoniflorin ameliorates ulcerative colitis by modulating the dendritic cell-mediated T(H)17/T(reg) balance.
Paeoniflorin ameliorates ulcerative colitis by modulating the dendritic cell-mediated T(H)17/T(reg) balance.
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芍药苷通过调节树突状细胞介导的 TH17/Treg 平衡改善溃疡性结肠炎
DOI：
10.1007/s10787-020-00722-6
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发表时间：
2020-12
影响因子：
5.8
通讯作者：
Yu J
中科院分区：
文献类型：
--
作者：
Zheng K;Jia J;Yan S;Shen H;Zhu P;Yu J
免疫耐受对于维持肠道稳态至关重要。产生白细胞介素 17 (IL-17) 的辅助性 T 细胞 17 (TH17) 与调节性 T 细胞 (Treg 细胞) 之间的不平衡与溃疡性结肠炎 (UC) 的发病机制有关。树突状细胞 (DC) 能够诱导 T 细胞分化。芍药苷 (PF) 是一种单萜葡萄糖苷，常用于治疗自身免疫性疾病。然而，PF参与UC治疗的免疫学机制尚不清楚。本研究旨在探讨PF是否可以通过调节DC来恢复TH17/Treg平衡。测量了 PF 对 DC、TH17 细胞和 Treg 细胞的影响。此外，将 PF 处理的 DC 注射到患有 2,4,6-三硝基苯磺酸 (TNBS) 诱导的结肠炎的小鼠体内。 PF 抑制 DC 表面 MHC-II 和 CD86 表达（P < 0.05），减少体内外白细胞介素（IL）-12 分泌（P < 0.05），并恢复结肠炎小鼠模型中的 TH17/Treg 比值（P < 0.05）。 PF处理的DC减少了TH17分化（体外4.26％，体内1.64％）并降低IL-17表达（P < 0.05），同时诱导CD4 + CD25 + Foxp3 + Treg分化（体外7.82％，体内6.85％）并增加Foxp3和IL-10产量（P < 0.05）。此外，PF 和 PF 处理的 DC 均改善了小鼠结肠炎模型中的结肠组织病理学（P < 0.05）。总之，本研究表明 PF 可以通过调节 DC 介导的 TH17/Treg 平衡来改善 TNBS 诱导的结肠炎。
Immunological tolerance is critical for maintaining gut homeostasis. An imbalance between interleukin-17 (IL-17)-producing T helper 17 (TH17) cells and regulatory T cells (Treg cells) is involved in ulcerative colitis (UC) pathogenesis. Dendritic cells (DCs) are able to induce T cell differentiation. Paeoniflorin (PF) is a monoterpene glucoside that is commonly used for treatment of autoimmune disease. However, the immunological mechanism of PF involvement in UC treatment is unclear. The present study aimed to explore whether PF can restore the TH17/Treg balance by modulating DCs. The effects of PF on DCs, TH17 cells and Treg cells were measured. Furthermore, PF-treated DCs were injected into mice with 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. PF inhibited MHC-II and CD86 expression on the DC surface (P 0.05), decreased interleukin (IL)-12 secretion in vitro and in vivo (P 0.05), and restored the TH17/Treg ratio in the mouse model of colitis (P 0.05). PF-treated DCs diminished TH17 differentiation (4.26% in vitro and 1.64% in vivo) and decreased IL-17 expression (P 0.05) while inducing CD4+CD25+Foxp3+ Treg differentiation (7.82% in vitro and 6.85% in vivo) and increasing Foxp3 and IL-10 production (P 0.05). Additionally, both PF and PF-treated DCs improved colonic histopathology in the mouse model of colitis (P 0.05). In conclusion this study suggested that PF can ameliorate TNBS-induced colitis by modulating the DC-mediated TH17/Treg balance.
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影响因子：
16.8
作者：
Iberg CA;Jones A;Hawiger D
通讯作者：
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影响因子：
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作者：
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影响因子：
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作者：
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影响因子：
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作者：
Ordas, Ingrid;Eckmann, Lars;Sandborn, William J.
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