4.7 Article

Lactobacillus paracasei L9 improves colitis by expanding butyrate-producing bacteria that inhibit the IL-6/STAT3 signaling pathway

Journal

FOOD & FUNCTION
Volume 12, Issue 21, Pages 10700-10713

Publisher

ROYAL SOC CHEMISTRY
DOI: 10.1039/d1fo02077c

Keywords

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Funding

  1. National Natural Science Foundation of China [81772984, 82025006, 82000498]
  2. China Postdoctoral Science Foundation [2020M680758]
  3. Basic Research Program [2019TC227, 2019TC088, 2021TC079]
  4. SKLAB Open Grant [2020SKLAB6-18]

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The study showed that the probiotic Lactobacillus paracasei L9 can alleviate the development of DSS-induced colitis by enhancing the abundance of butyrate-producing bacterial strains. The mechanism involves butyrate suppressing the IL-6/STAT3 signaling pathway to ameliorate inflammatory responses in colitis. This provides new insight into a potential therapeutic target for IBD remission.
Inflammatory bowel disease (IBD) is a chronic intestinal inflammation that is currently incurable. Increasing evidence indicates that supplementation with probiotics could improve the symptoms of IBD. It is scientifically significant to identify novel and valid strains for treating IBD. It has been reported that the probiotic Lactobacillus paracasei L9 (L9), which is identified from the gut of healthy centenarians, can modulate host immunity and plays an anti-allergic role. Here, we demonstrated that L9 alleviates the pathological phenotypes of experimental colitis by expanding the abundance of butyrate-producing bacteria. Oral administration of sodium butyrate in experimental colitis recapitulates the L9 anti-inflammatory phenotypes. Mechanistically, sodium butyrate ameliorated the inflammatory responses by inhibiting the IL-6/STAT3 signaling pathway in colitis. Overall, these findings demonstrated that L9 alleviates the DSS-induced colitis development by enhancing the abundance of butyrate-producing bacterial strains that produce butyrate to suppress the IL-6/STAT3 signaling pathway, providing new insight into a promising therapeutic target for the remission of IBD.

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