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SDF-1/CXCR4 轴增强人子宫内膜再生细胞的免疫调节作用，缓解实验性结肠炎。

SDF-1/CXCR4 axis enhances the immunomodulation of human endometrial regenerative cells in alleviating experimental colitis.

机构信息

Department of General Surgery, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin, 300052, China.

Tianjin General Surgery Institute, Tianjin, China.

出版信息

Stem Cell Res Ther. 2019 Jul 8;10(1):204. doi: 10.1186/s13287-019-1298-6.

DOI:10.1186/s13287-019-1298-6
PMID:31286993
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6615145/
Abstract

Endometrial regenerative cells (ERCs) are a new type of mesenchymal-like stromal cells, and their therapeutic potential has been tested in a variety of disease models. SDF-1/CXCR4 axis plays a chemotaxis role in stem/stromal cell migration. The aim of the present study was to investigate the role of SDF-1/CXCR4 axis in the immunomodulation of ERCs on the experimental colitis. The immunomodulation of ERCs in the presence or absence of pretreatment of SDF-1 or AMD3100 was examined in both in vitro cell culture system and dextran sulphate sodium-induced colitis in mice. The results showed that SDF-1 increased the expression of CXCR4 on the surface of ERCs. As compared with normal ERCs, the SDF-1-treated, CXCR4 high-expressing ERCs more significantly suppressed dendritic cell population as well as stimulated both type 2 macrophages and regulatory T cells in vitro and in vivo. Meanwhile, SDF-1-pretreated ERCs increased the generation of anti-inflammatory factors (e.g., IL-4, IL-10) and decreased the pro-inflammatory factors (e.g., IL-6, TNF-α). In addition, SDF-1-pretreated CM-Dil-labeled ERCs were found to engraft to injured colon. Our results may suggest that an SDF-1-induced high level of CXCR4 expression enhances the immunomodulation of ERCs in alleviating experimental colitis in mice.

摘要

子宫内膜再生细胞（ERCs）是一种新型的间充质样基质细胞，其治疗潜力已在多种疾病模型中得到测试。SDF-1/CXCR4 轴在干细胞/基质细胞迁移中发挥趋化作用。本研究旨在探讨 SDF-1/CXCR4 轴在 ERC 对实验性结肠炎的免疫调节中的作用。在体外细胞培养系统和葡聚糖硫酸钠诱导的小鼠结肠炎中，研究了 SDF-1 预处理或 AMD3100 预处理对 ERC 免疫调节的影响。结果表明，SDF-1 增加了 ERC 表面 CXCR4 的表达。与正常 ERC 相比，SDF-1 处理的 CXCR4 高表达 ERCs 在体外和体内更显著地抑制树突状细胞群体，并刺激 2 型巨噬细胞和调节性 T 细胞。同时，SDF-1 预处理的 ERCs 增加了抗炎因子（如 IL-4、IL-10）的产生，减少了促炎因子（如 IL-6、TNF-α）的产生。此外，发现 SDF-1 预处理的 CM-Dil 标记的 ERCs 定植到受损的结肠。我们的结果可能表明，SDF-1 诱导的 CXCR4 表达水平升高增强了 ERCs 的免疫调节作用，从而缓解了小鼠实验性结肠炎。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3521/6615145/b2a1c4459dfc/13287_2019_1298_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3521/6615145/d25d2fabd76e/13287_2019_1298_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3521/6615145/6c58992795fa/13287_2019_1298_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3521/6615145/3dc409249dbf/13287_2019_1298_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3521/6615145/d8b4706f17aa/13287_2019_1298_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3521/6615145/a846c70ecf54/13287_2019_1298_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3521/6615145/b2a1c4459dfc/13287_2019_1298_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3521/6615145/d25d2fabd76e/13287_2019_1298_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3521/6615145/6c58992795fa/13287_2019_1298_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3521/6615145/3dc409249dbf/13287_2019_1298_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3521/6615145/d8b4706f17aa/13287_2019_1298_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3521/6615145/a846c70ecf54/13287_2019_1298_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3521/6615145/b2a1c4459dfc/13287_2019_1298_Fig6_HTML.jpg

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