Sodium selenite ameliorates dextran sulfate sodium-induced chronic colitis in mice by decreasing Th1, Th17, and γδT and increasing CD4(+)CD25(+) regulatory T-cell responses.
Sodium selenite ameliorates dextran sulfate sodium-induced chronic colitis in mice by decreasing Th1, Th17, and γδT and increasing CD4(+)CD25(+) regulatory T-cell responses.
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亚硒酸钠通过降低 Th1、Th17 和 γ δ T 并增加 CD4( ) CD25( ) 调节性 T 细胞反应，改善右旋糖酐硫酸钠诱导的小鼠慢性结肠炎
DOI：
10.3748/wjg.v23.i21.3850
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发表时间：
2017-06-07
影响因子：
4.3
通讯作者：
Sun X
中科院分区：
文献类型：
--
作者：
Sang LX;Chang B;Zhu JF;Yang FL;Li Y;Jiang XF;Wang DN;Lu CL;Sun X
目的：探讨亚硒酸钠对葡聚糖硫酸钠(DSS)诱导的C57BL/6小鼠结肠炎的影响。将小鼠随机分为4组(n=10/组)：正常组、硒(Se)组、慢性结肠炎组、Se+慢性结肠炎组。于第26天处死小鼠。测定存活率、临床症状、结肠长度和组织学改变。测定结肠固有层淋巴细胞(LPL)免疫细胞百分率和绝对数、结肠组织中mRNA的表达以及结肠LPL中Th1、Th17和Treg细胞因子的浓度。硒显著改善结肠炎症状和组织学损伤(P均0.05)，升高中性粒细胞和CD_4~+CD25~+T细胞的比例(P均0.05)，降低γδT细胞、CD_4~+、CD_4~+CD_4 4~+和CD_4~+CD_(69)~+T细胞的比例(P均0.05)。此外，Se还可降低IL-6、干扰素-γ、IL-17A、IL-21、T-bet和RoRγt的表达(P均<0.05)，但增强IL-10和Foxp3的表达(P均<0.05)。这些结果表明，Se对DSS诱导的慢性结肠炎有保护作用，可能是通过增加抑制促炎细胞因子分泌的CD_4(+)CD_(25)T细胞的数量和Th1、Th17和γδT细胞的数量。
To assess the effect of sodium selenite on the severity of dextran sulfate sodium (DSS)-induced colitis in C57BL/6 mice. Mice were randomly divided into four groups (n = 10/group): normal group, selenium (Se) group, chronic colitis group, and Se + chronic colitis group. The mice were sacrificed on day 26. Survival rates, clinical symptoms, colon length, and histological changes were determined. The percentages and absolute numbers of immune system cells in the lamina propria lymphocytes (LPL) of the colon, the expression of mRNA in colon tissue, and the concentrations of Th1, Th17, and Treg cytokines in LPL from the large intestine, were measured. Se significantly ameliorated the symptoms of colitis and histological injury (P < 0.05 each), increasing the proportions of neutrophils and CD4+ CD25+ T cells (P < 0.05 each) and decreasing the proportions of γδT cells, CD4+, CD4+CD44+, and CD4+ CD69+ T cells in LPL (P < 0.05 each). Moreover, Se reduced the expression of IL-6, IFN-γ, IL-17A, IL-21, T-bet, and RORγt (P < 0.05 each), but enhanced the expression of IL-10 and Foxp3 (P < 0.05 each). These results suggest that Se protects against DSS-induced chronic colitis perhaps by increasing the number of CD4(+)CD25(+) Tregs that suppress the secretion of proinflammatory cytokines and populations of Th1, Th17, and γδT cells.