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肠系膜淋巴结：在结肠炎治疗中通过产生 TGF-β1，hUC-MSCs 对 Treg 细胞的上调作用的关键部位。

Mesenteric lymph nodes: a critical site for the up-regulatory effect of hUC-MSCs on Treg cells by producing TGF-β1 in colitis treatment.

机构信息

Key Laboratory of Drug Metabolism and Pharmacokinetics, Haihe Laboratory of Cell Ecosystem, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, China.

Jiangsu Renocell Biotech Co., Ltd, Nanjing, China.

出版信息

Stem Cell Res Ther. 2024 Jul 2;15(1):190. doi: 10.1186/s13287-024-03809-x.

DOI:10.1186/s13287-024-03809-x
PMID:38956621
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11218300/
Abstract

BACKGROUND: Mesenchymal stem cells (MSCs) demonstrate a wide range of therapeutic capabilities in the treatment of inflammatory bowel disease (IBD). The intraperitoneal injection of MSCs has exhibited superior therapeutic efficacy on IBD than intravenous injection. Nevertheless, the precise in vivo distribution of MSCs and their biological consequences following intraperitoneal injection remain inadequately understood. Additional studies are required to explore the correlation between MSCs distribution and their biological effects. METHODS: First, the distribution of human umbilical cord MSCs (hUC-MSCs) and the numbers of Treg and Th17 cells in mesenteric lymph nodes (MLNs) were analyzed after intraperitoneal injection of hUC-MSCs. Subsequently, the investigation focused on the levels of transforming growth factor beta1 (TGF-β1), a key cytokine to the biology of both Treg and Th17 cells, in tissues of mice with colitis, particularly in MLNs. The study also delved into the impact of hUC-MSCs therapy on Treg cell counts in MLNs, as well as the consequence of TGFB1 knockdown hUC-MSCs on the differentiation of Treg cells and the treatment of IBD. RESULTS: The therapeutic effectiveness of intraperitoneally administered hUC-MSCs in the treatment of colitis was found to be significant, which was closely related to their quick migration to MLNs and secretion of TGF-β1. The abundance of hUC-MSCs in MLNs of colitis mice is much higher than that in other organs even the inflamed sites of colon. Intraperitoneal injection of hUC-MSCs led to a significant increase in the number of Treg cells and a decrease in Th17 cells especially in MLNs. Furthermore, the concentration of TGF-β1, the key cytokine for Treg differentiation, were also found to be significantly elevated in MLNs after hUC-MSCs treatment. Knockdown of TGFB1 in hUC-MSCs resulted in a noticeable reduction of Treg cells in MLNs and the eventually failure of hUC-MSCs therapy in colitis. CONCLUSIONS: MLNs may be a critical site for the regulatory effect of hUC-MSCs on Treg/Th17 cells and the therapeutic effect on colitis. TGF-β1 derived from hUC-MSCs promotes local Treg differentiation in MLNs. This study will provide new ideas for the development of MSC-based therapeutic strategies in IBD patients.

摘要

背景：间充质干细胞（MSCs）在治疗炎症性肠病（IBD）方面表现出广泛的治疗能力。与静脉注射相比，腹腔内注射 MSCs 对 IBD 具有更好的治疗效果。然而，腹腔内注射后 MSCs 的确切体内分布及其生物学后果仍了解不足。需要进一步研究来探讨 MSCs 分布与生物学效应之间的相关性。

方法：首先，分析了腹腔内注射人脐带间充质干细胞（hUC-MSCs）后 hUC-MSCs 在肠系膜淋巴结（MLNs）中的分布以及 Treg 和 Th17 细胞的数量。随后，研究集中于转化生长因子β 1（TGF-β1）的水平，TGF-β1 是 Treg 和 Th17 细胞生物学的关键细胞因子，尤其是在结肠炎小鼠的 MLNs 组织中。该研究还探讨了 hUC-MSCs 治疗对 MLNs 中 Treg 细胞计数的影响，以及 TGFB1 敲低 hUC-MSCs 对 Treg 细胞分化和 IBD 治疗的影响。

结果：腹腔内给予 hUC-MSCs 治疗结肠炎的疗效显著，这与它们迅速迁移到 MLNs 并分泌 TGF-β1 密切相关。结肠炎小鼠 MLNs 中 hUC-MSCs 的丰度明显高于其他器官，甚至是发炎的结肠部位。腹腔内注射 hUC-MSCs 可显著增加 Treg 细胞数量并减少 Th17 细胞，尤其是在 MLNs 中。此外，hUC-MSCs 治疗后 MLNs 中 TGF-β1（Treg 分化的关键细胞因子）的浓度也明显升高。hUC-MSCs 中 TGFB1 的敲低导致 MLNs 中 Treg 细胞数量明显减少，最终导致 hUC-MSCs 治疗结肠炎失败。

结论：MLNs 可能是 hUC-MSCs 对 Treg/Th17 细胞的调节作用和对结肠炎的治疗作用的关键部位。来自 hUC-MSCs 的 TGF-β1 促进 MLNs 中局部 Treg 分化。这项研究将为 IBD 患者基于 MSC 的治疗策略的发展提供新的思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c66a/11218300/5831c93eaf7c/13287_2024_3809_Fig7_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c66a/11218300/4d388635c426/13287_2024_3809_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c66a/11218300/363df2900b30/13287_2024_3809_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c66a/11218300/5831c93eaf7c/13287_2024_3809_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c66a/11218300/357611a1302e/13287_2024_3809_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c66a/11218300/292e1a49d567/13287_2024_3809_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c66a/11218300/ba00c3ff583f/13287_2024_3809_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c66a/11218300/e5f4772d2552/13287_2024_3809_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c66a/11218300/4d388635c426/13287_2024_3809_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c66a/11218300/363df2900b30/13287_2024_3809_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c66a/11218300/5831c93eaf7c/13287_2024_3809_Fig7_HTML.jpg

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引用本文的文献

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Front Immunol. 2025-6-4

[2]
Novel Insights into the Pathogenesis of Inflammatory Bowel Diseases.

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[3]
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Stem Cell Res Ther. 2024-11-28

[4]
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Signal Transduct Target Ther. 2024-11-18

本文引用的文献

[1]
Human umbilical cord mesenchymal stem cells ameliorate colon inflammation via modulation of gut microbiota-SCFAs-immune axis.

Stem Cell Res Ther. 2023-9-25

[2]
Nongenetic surface engineering of mesenchymal stromal cells with polyvalent antibodies to enhance targeting efficiency.

Nat Commun. 2023-9-19

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Intricacies of TGF-β signaling in Treg and Th17 cell biology.

Cell Mol Immunol. 2023-9

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TGF-β Regulation of T Cells.

Annu Rev Immunol. 2023-4-26

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Therapeutic potential of mesenchymal stem/stromal cells (MSCs)-based cell therapy for inflammatory bowel diseases (IBD) therapy.

Eur J Med Res. 2023-1-27

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Salidroside alleviates ulcerative colitis via inhibiting macrophage pyroptosis and repairing the dysbacteriosis-associated Th17/Treg imbalance.

Phytother Res. 2023-2

[7]
Qing-Chang-Hua-Shi granule ameliorates DSS-induced colitis by activating NLRP6 signaling and regulating Th17/Treg balance.

Phytomedicine. 2022-12

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Mechanisms of mucosal healing: treating inflammatory bowel disease without immunosuppression?

Nat Rev Gastroenterol Hepatol. 2022-8

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Treatment of Inflammatory Bowel Disease: A Comprehensive Review.

Front Med (Lausanne). 2021-12-20

[10]
Stigmasterol Restores the Balance of Treg/Th17 Cells by Activating the Butyrate-PPARγ Axis in Colitis.

Front Immunol. 2021

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