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血管活性肠肽通过调节 Th17/Treg 平衡改善了 1-十六烷醇诱导的狼疮小鼠模型的肾损伤。

Vasoactive intestinal peptide ameliorates renal injury in a pristane-induced lupus mouse model by modulating Th17/Treg balance.

机构信息

Department of Nephrology, Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18 Zhongshan Road II, Baise, 533000, Guangxi Zhuang Autonomous Region, China.

出版信息

BMC Nephrol. 2019 Sep 5;20(1):350. doi: 10.1186/s12882-019-1548-y.

DOI:10.1186/s12882-019-1548-y
PMID:31488076
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6728947/
Abstract

BACKGROUND

Lupus nephritis (LN) is an inflammation of the kidneys and is a major cause of mortality in systemic lupus erythaematosus (SLE) patients. In addition, Th17/Treg balance is one of the most important factors that can promote the development of LN. It has been reported that vasoactive intestinal peptide (VIP) is associated with the downregulation of both inflammatory and autoimmune diseases through regulating T lymphocyte balance. Therefore, the aim of this study was to determine the role of VIP in modulating Th17/Treg balance in LN.

METHODS

LN was induced in BALB/c female mice by injection pristane. After 3 months, mice were randomly divided into four groups: control, VIP + control, LN and VIP + LN. Autoantibody levels were tested by ELISA. The distribution of Th17/Treg cells in vivo and in vitro was detected by FC. Renal tissues were examined by PASM and DIF for pathology and Foxp3CD3. The mRNA and protein expression levels of pro- and anti-inflammatory cytokines were detected by qRT-PCR and western blotting.

RESULTS

VIP can improve renal injury by regulating Th17/Treg imbalance in LN mice. Proteinuria, renal function defects and autoantibodies were significantly decreased, and Th17/Treg cell balance was restored in VIP compared with LN mice. In addition, VIP improved renal lesions by promoting the expression of Foxp3CD3 in renal tissue. Furthermore, VIP downregulated the mRNA and protein expression of IL-17, IL-6 and upregulated Foxp3, IL-10 expression.

CONCLUSIONS

VIP reduced LN proteinuria and renal function defects and restored the Th17/Treg cell balance. Furthermore, VIP also downregulated autoantibody and inflammatory cytokine expression and upregulated Foxp3 and IL-10 expression.

摘要

背景

狼疮肾炎（LN）是肾脏炎症，是系统性红斑狼疮（SLE）患者死亡的主要原因。此外，Th17/Treg 平衡是促进 LN 发展的最重要因素之一。据报道，血管活性肠肽（VIP）通过调节 T 淋巴细胞平衡与炎症和自身免疫性疾病的下调有关。因此，本研究旨在确定 VIP 在调节 LN 中 Th17/Treg 平衡中的作用。

方法

通过注射降植烷诱导 BALB/c 雌性小鼠 LN。3 个月后，将小鼠随机分为四组：对照组、VIP+对照组、LN 组和 VIP+LN 组。通过 ELISA 检测自身抗体水平。通过 FC 检测体内和体外 Th17/Treg 细胞的分布。PASM 和 DIF 检查肾脏组织病理学和 Foxp3CD3。通过 qRT-PCR 和 Western blot 检测促炎和抗炎细胞因子的 mRNA 和蛋白表达水平。

结果

VIP 通过调节 LN 小鼠的 Th17/Treg 失衡可改善肾脏损伤。与 LN 组相比，VIP 组蛋白尿、肾功能缺陷和自身抗体明显减少，Th17/Treg 细胞平衡得到恢复。此外，VIP 通过促进肾组织中 Foxp3CD3 的表达改善了肾脏病变。此外，VIP 下调了 IL-17、IL-6 的 mRNA 和蛋白表达，上调了 Foxp3 和 IL-10 的表达。

结论

VIP 减少 LN 蛋白尿和肾功能缺陷，恢复 Th17/Treg 细胞平衡。此外，VIP 还下调了自身抗体和炎症细胞因子的表达，上调了 Foxp3 和 IL-10 的表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec4f/6728947/5ea409a38118/12882_2019_1548_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec4f/6728947/b1f37cfd6b48/12882_2019_1548_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec4f/6728947/0c6d3aa06aa9/12882_2019_1548_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec4f/6728947/cdf80a7b6507/12882_2019_1548_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec4f/6728947/2f98be51a8e2/12882_2019_1548_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec4f/6728947/d3138037b497/12882_2019_1548_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec4f/6728947/5ea409a38118/12882_2019_1548_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec4f/6728947/b1f37cfd6b48/12882_2019_1548_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec4f/6728947/0c6d3aa06aa9/12882_2019_1548_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec4f/6728947/cdf80a7b6507/12882_2019_1548_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec4f/6728947/2f98be51a8e2/12882_2019_1548_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec4f/6728947/d3138037b497/12882_2019_1548_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec4f/6728947/5ea409a38118/12882_2019_1548_Fig6_HTML.jpg

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