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Lactobacillus paracasei Jlus66 relieves DSS-induced ulcerative colitis in a murine model by maintaining intestinal barrier integrity, inhibiting inflammation, and improving intestinal microbiota structure

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Ulcerative colitis (UC) is a serious health problem with increasing morbidity and prevalence worldwide. The pathogenesis of UC is complex, currently believed to be influenced by genetic factors, dysregulation of the host immune system, imbalance in the intestinal microbiota, and environmental factors. Currently, UC is typically managed using aminosalicylates, immunosuppressants, and biologics as adjunctive therapies, with the risk of relapse and development of drug resistance upon discontinuation. Therefore, further research into the pathogenesis of UC and exploration of potential treatment strategies are necessary to improve the quality of life for affected patients. According to previous studies, Lactobacillus paracasei Jlus66 (Jlus66) reduced inflammation and may help prevent or treat UC.


We used dextran sulfate sodium (DSS) to induce a mouse model of UC to assess the effect of Jlus66 on the progression of colitis. During the experiment, we monitored mouse body weight, food and water consumption, as well as rectal bleeding. Hematoxylin-eosin staining was performed to assess intestinal pathological damage. Protein imprinting and immunohistochemical methods were used to evaluate the protein levels of nuclear factor-kappa B (NF-κB), mitogen-activated protein kinase (MAPK), and tight junction (TJ) proteins in intestinal tissues. Fecal microbiota was analyzed based on partial 16S rRNA gene sequencing.


Jlus66 supplementation reduced the degree of colon tissue damage, such as colon shortening, fecal occult blood, colon epithelial damage, and weight loss. Supplementation with Jlus66 reduced DSS-induced upregulation of cytokine levels such as TNF-α, IL-1β, and IL-6 (p < 0.05). The NF-κB pathway and MAPK pathway were inhibited, and the expression of TJ proteins (ZO-1, Occludin, and Claudin-3) was upregulated. 16S rRNA sequencing of mouse cecal contents showed that Jlus66 effectively regulated the structure of the intestinal biota.


In conclusion, these data indicate that Jlus66 can alter the intestinal biota and slow the progression of UC, providing new insights into potential therapeutic strategies for UC.

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Data availability

The datasets used and analysed in this current study are available from the corresponding author upon reasonable request.



Ulcerative Colitis


Dextran Sulfate Sodium


Haematoxylin and Eosin


Tumor Necrosis Factor




Glyceraldehyde-3-phosphate dehydrogenase


Colony Forming Unit


Alcian Blue-Periodic Acid Schif


Nuclear Factor-Kappa B


Mitogen-Activated Protein Kinase


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This work was supported by the National Key Research and Development Program of China (No.2023YFD1801000) and the Interdisciplinary Integration and Innovation Project of JLU (No. JLUXKJC2021ZY08).

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Correspondence to Pan Hu.

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All experimental procedures were performed according to the guidelines of Animal Investigation Ethics Committee in Jilin University (No. SY202010004). They were therefore performed in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki and its later amendments.

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Yu, F., Wang, X., Ren, H. et al. Lactobacillus paracasei Jlus66 relieves DSS-induced ulcerative colitis in a murine model by maintaining intestinal barrier integrity, inhibiting inflammation, and improving intestinal microbiota structure. Eur J Nutr (2024).

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