ArticlePLoS neglected tropical diseases2024
Hymenolepis nana antigens alleviate ulcerative colitis by promoting intestinal stem cell proliferation and differentiation via AhR/IL-22 signaling pathway.
Article in PLoS neglected tropical diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Risk of Inflammatory Bowel Disease Following Hospital-Treated Infections and Modulatory Role of Host Genetics to Support a Multi-Hit Pathogenesis Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- TiO2 eliminates Hymenolepis nana eggs via photocatalytic activity.PLoS neglected tropical diseases · 2025Article
- Excretory/secretory products from Hymenolepis nana adult worms alleviate ulcerative colitis in mice via tuft/IL-13 signaling pathway.Parasites & vectors · 2025Article
- Potential applications and mechanisms of natural products in mucosal-related diseases.Frontiers in immunology · 2025Review
- The AhR/IL-22 axis in chronic gut inflammation: unraveling mechanisms and therapeutic prospects.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.