4.7 Article

Lactobacillus paracasei R3 protects against dextran sulfate sodium (DSS)-induced colitis in mice via regulating Th17/Treg cell balance

期刊

JOURNAL OF TRANSLATIONAL MEDICINE
卷 19, 期 1, 页码 -

出版社

BMC
DOI: 10.1186/s12967-021-02943-x

关键词

Lactobacillus paracasei; Colitis; Dextran sulfate sodium; Treg; Th17; Whole genome sequencing

资金

  1. Natural Science Foundation of Guangdong Province [2019A1515011713]
  2. Medical Science Foundation of Guangdong Province [B2018014, A2020211]
  3. Key Cultivation Project of Guangdong Medical University [GDMUZ2019001]
  4. Discipline Construction Project of Guangdong Medical University [4SG21278P]
  5. Guangdong Medical University Student Innovation Experiment Project [GDMU2019132, ZZDC001, ZYDG002]
  6. Research Foundation of Guangdong Medical University [M2017012, GDMUM2020006]
  7. Guangdong Province Science and Technology Innovation Strategy Special Fund [pdjh2020b0268]

向作者/读者索取更多资源

This study demonstrates that the L.p R3 strain significantly improves symptoms and pathological damage in mice with colitis, and influences immune function by regulating the Th17/Treg cell balance in DSS-induced colitis in mice.
Inflammatory bowel diseases (IBD), mainly comprising ulcerative colitis (UC) and Crohn's Disease, are most often a polygenic disorder with contributions from the intestinal microbiome, defects in barrier function, and dysregulated host responses to microbial stimulation. Strategies that target the microbiota have emerged as potential therapies and, of these, probiotics have gained the greatest attention. Herein, we isolated a strain of Lactobacillus paracasei R3 (L.p R3) with strong biofilm formation ability from infant feces. Interestingly, we also found L.p R3 strain can ameliorate the general symptoms of murine colitis, alleviate inflammatory cell infiltration and inhibit Th17 while promote Treg function in murine dextran sulfate sodium (DSS)-induced colitis. Overall, this study suggested that L.p R3 strain significantly improves the symptoms and the pathological damage of mice with colitis and influences the immune function by regulating Th17/Treg cell balance in DSS-induced colitis in mice.

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