Laquinimod ameliorates spontaneous colitis in interleukin-10-gene-deficient mice with improved barrier function

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Background and aims:

Crohn's disease is an autoimmune disease associated with imbalanced mucosal immunity, mediated with increased Th1 and Th17 cells. Laquinimod, an immunomodulatory drug, has shown efficacy in regulating the differentiation of T cells. The aim of the study was to investigate the therapeutic effect of laquinimod on spontaneous colitis in interleukin-10-gene-deficient mice, an animal model of Crohn's disease.


Male Il10−/− mice aged 16 weeks in the laquinimod group were treated with laquinimod with distilled water at a dose of 25 mg/kg by oral gavage, 3 times a week. Il10−/− mice in the IL-10-KO group and wild type mice received equal volume of phosphate buffered saline by oral gavage, 3 times a week. After 4 weeks, mice were sacrificed for analysis. Severity of colitis, epithelial expression of T-cell-associated cytokines, expression and distribution of tight junction proteins in the lamina propria and NF-κB signaling pathway associated mRNA expression were measured at the end of the experiment.


Laquinimod treatment ameliorated spontaneous colitis in Il10−/− mice, which was associated with decreased T-cell-associated pro-inflammatory cytokines. Increased expression and correct distribution of tight junction proteins (occludin and ZO-1) were found in Il10−/− mice treated with laquinimod. In addition, in mice treated with laquinimod, NF-κB signaling pathway associated mRNA in the colon was also downregulated.


Our results indicated that laquinimod treatment ameliorates colitis in Il10−/− mice and improves intestinal barrier function, which may support a new therapeutic approach to Crohn's disease.

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