ORIGINAL RESEARCH article
Front. Immunol.
Sec. Parasite Immunology
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1600838
This article is part of the Research TopicHelminthosis: Immuno-pathology and Anthelmintic VaccinesView all 9 articles
Protective Effects of Nippostrongylus brasiliensis-Derived Uridine via the Apical Sodium-Dependent Bile Acid Transporter in a Mouse Model of TNBS-Induced Inflammatory Bowel Disease
Provisionally accepted- 1Nanjing Medical University, Nanjing, Jiangsu Province, China
- 2Jiangsu Institute of Parasitic Diseases (JIPD), Wuxi, China
- 3Guangzhou Tianhe District Center for Disease Control and Prevention, Guangzhou, China
- 4Wuxi Xishan People′s Hospital, Jangsu, China
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Colitis, is a chronic immune-mediated gastrointestinal disorder with unclear etiology. Current therapies often fail to achieve complete remission, making it necessary to explore novel therapeutic strategies. The hygiene hypothesis suggests that helminth infections may modulate immune responses, offering potential benefits for inflammatory diseases. Nippotrongylus brasiliensis (Nb), a hookworm-like nematode, secrets immunoregulatory molecules, including uridine, which exhibits anti-inflammatory properties. Here, we investigated the protective effects of Nb infection, its excretory-secretory (ES) products, and uridine in a TNBS-induced IBD mouse model. Moreover, we conducted an RNA sequencing (RNA-Seq) analysis to elucidate the possible functional mechanisms for the protective effects of ES or uridine. Results demonstrated that uridine can exhibit a protective effect on TNBS-induced IBD in mice. RNA-Seq revealed that uridine upregulated slc10a2, encoding the apical sodium-dependent bile acid transporter (ASBT). By pharmacological inhibition of the encoding protein (ASBT), its impact on the protective efficacy has been abolished.Our findings demonstrate that uridine alleviates IBD by modulating ASBT, suggesting a novel therapeutic target for IBD intervention.
Keywords: Nippostrongylus brasiliensis, Uridine, Apical sodium-dependent bile acid transporter, inflammatory bowel disease, RNA sequencing
Received: 27 Mar 2025; Accepted: 09 Apr 2025.
Copyright: © 2025 Yuan, Wang, Chen, Ding, Zhang, Yao, Zhang, Bai and Dai. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Hongxia Bai, Wuxi Xishan People′s Hospital, Jangsu, 214011, China
Yang Dai, Jiangsu Institute of Parasitic Diseases (JIPD), Wuxi, China
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