4.6 Article

Monosexual Cercariae of Schistosoma japonicum Infection Protects Against DSS-Induced Colitis by Shifting the Th1/Th2 Balance and Modulating the Gut Microbiota

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FRONTIERS IN MICROBIOLOGY
卷 11, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fmicb.2020.606605

关键词

inflammatory bowel disease; monosexual cercariae; Schistosoma japonicum; Th1/Th2; gut microbiota

资金

  1. National Natural Science Foundation of China [81572023, 81371836]
  2. Key Research and Development Program of Hainan Province [ZDYF2020120]
  3. Guangdong Natural Science Foundation [2019A1515011541]
  4. Science and Technology Planning Project of Guangdong Province [2019B030316025]
  5. National Parasitic Resources Center of China [NPRC-2019-19430]
  6. Open Foundation of Key Laboratory of Tropical Translational Medicine of the Ministry of Education, Hainan Medical University [2020TTM007]
  7. 111 Project [B12003]
  8. Teaching Reform Project of Guangdong Province [2017001]

向作者/读者索取更多资源

This study investigated the therapeutic effects of monosexual Schistosoma japonicum cercariae and dexamethasone on inflammatory bowel disease using a mouse model. The results showed that monosexual Schistosoma japonicum cercariae could alleviate clinical symptoms of inflammatory bowel disease and improve intestinal permeability by modulating the Th1/Th2 balance, Treg cell population, and reshaping the gut microbiota community.
Inflammatory bowel disease (IBD)-related inflammation is closely associated with the initiation and progression of colorectal cancer. IBD is generally treated with 5-aminosalicylic acid and immune-modulating medication, but side effects and limitations of these therapies are emerging. Thus, the development of novel preventative or therapeutic approaches is imperative. Here, we constructed a dextran sodium sulphate (DSS)-induced IBD mouse model that was infected with monosexual Schistosoma japonicum cercariae (mSjci) at day 1 or administered dexamethasone (DXM) from days 3 to 5 as a positive control. The protective effect of mSjci on IBD mice was evaluated through their assessments of their clinical signs, histopathological lesions and intestinal permeability. To uncover the underlying mechanism, the Th1/Th2 balance and Treg cell population were also examined. Additionally, the alterations in the gut microbiota were assessed to investigate the interaction between the mSjci-modulated immune response and pathogenic microbiome. Mice treated with DSS and mSjci showed fewer IBD clinical signs and less impaired intestinal permeability than DSS-treated mice. Mechanistically, mSjci modulated the Th1/Th2 balance by repressing IFN-gamma production, promoting IL-10 expression and enhancing the Treg subset population. Moreover, mSjci notably reshaped the structure, diversity and richness of the gut microbiota community and subsequently exerted immune-modulating effects. Our findings provide evidence showing that mSjci might serve as a novel and effective protective strategy and that the gut microbiota might be a new therapeutic target in IBD.

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