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微小膜壳绦虫抗原通过AhR/IL-22信号通路促进肠干细胞增殖和分化来缓解溃疡性结肠炎。

Hymenolepis nana antigens alleviate ulcerative colitis by promoting intestinal stem cell proliferation and differentiation via AhR/IL-22 signaling pathway.

作者信息

Cui Xuanyin, Cheng Yi, Wang Hongyan, Li Xiaomao, Li Jinfu, Zhang Ke, Mou Rong

机构信息

Guizhou Key Laboratory of Microbio and Infectious Disease Prevention & Control / The Key and Characteristic Laboratory of Modern Pathogenicity Biology, Department of Human Parasitology, School of Basic Medicine, Guizhou Medical University, Guiyang, China.

出版信息

PLoS Negl Trop Dis. 2024 Dec 12;18(12):e0012714. doi: 10.1371/journal.pntd.0012714. eCollection 2024 Dec.

DOI:10.1371/journal.pntd.0012714
PMID:39666730
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11670978/
Abstract

Ulcerative colitis (UC) is a chronic inflammatory bowel disease with an unknown etiology and is difficult to treat. Studies have shown that some helminths and their associated products have therapeutic potential in controlling or preventing inflammatory diseases. This study is to investigate the mitigation effects of Hymenolepis nana antigens (HnAg) on the UC model. HnAg significantly improved the disease activity index, colon length, and colonic pathological damage in mice with dextran sulfate sodium (DSS)-induced colitis. HnAg intervention could protect the number of goblet cells and enhance the expression of tight junction proteins and mucins, thereby improving intestinal barrier integrity. HnAg attenuated small intestinal organoid damage and stimulated intestinal stem cells proliferation in a DSS-induced mouse organoid inflammation model. The protective mechanism of HnAg might be related to the activation of the aryl hydrocarbon receptor (AhR)/IL-22 signaling pathway, which regulates intestinal barrier function and promotes the proliferation and differentiation of intestinal stem cells. In conclusion, HnAg has a therapeutic effect on UC mice. Our study provides a new approach for alleviating UC by Hymenolepis nana and its associated products.

摘要

溃疡性结肠炎（UC）是一种病因不明的慢性炎症性肠病，难以治疗。研究表明，一些蠕虫及其相关产物在控制或预防炎症性疾病方面具有治疗潜力。本研究旨在探讨微小膜壳绦虫抗原（HnAg）对UC模型的缓解作用。HnAg显著改善了葡聚糖硫酸钠（DSS）诱导的结肠炎小鼠的疾病活动指数、结肠长度和结肠病理损伤。HnAg干预可保护杯状细胞数量，增强紧密连接蛋白和黏蛋白的表达，从而改善肠道屏障完整性。在DSS诱导的小鼠类器官炎症模型中，HnAg减轻了小肠类器官损伤并刺激了肠道干细胞增殖。HnAg的保护机制可能与芳烃受体（AhR）/IL-22信号通路的激活有关，该信号通路调节肠道屏障功能并促进肠道干细胞的增殖和分化。总之，HnAg对UC小鼠具有治疗作用。我们的研究为微小膜壳绦虫及其相关产物缓解UC提供了一种新方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/11670978/dd41edd6e2f6/pntd.0012714.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/11670978/31da7623527b/pntd.0012714.g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/11670978/c2c1abe26dfe/pntd.0012714.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/11670978/0185520f2131/pntd.0012714.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/11670978/dd41edd6e2f6/pntd.0012714.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/11670978/31da7623527b/pntd.0012714.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/11670978/f50d186715d1/pntd.0012714.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/11670978/704542d0ed9d/pntd.0012714.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/11670978/32b40c8c48c1/pntd.0012714.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/11670978/f1d819800a36/pntd.0012714.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/11670978/7124c91a2eb9/pntd.0012714.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/11670978/c2c1abe26dfe/pntd.0012714.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/11670978/0185520f2131/pntd.0012714.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/11670978/dd41edd6e2f6/pntd.0012714.g009.jpg

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