Chen, Shih-YaoShih-YaoChenChu, Chun-TingChun-TingChuYang, Mei-LinMei-LinYangJIAN-DA LINWang, Chung-TengChung-TengWangLee, Che-HsinChe-HsinLeeLin, I-ChenI-ChenLinShiau, Ai-LiAi-LiShiauLing, PinPinLingWu, Chao-LiangChao-LiangWu2023-07-242023-07-242023-06-082076-2607https://scholars.lib.ntu.edu.tw/handle/123456789/634038The imbalance of mucosal immunity in the lower gastrointestinal tract can lead to chronic inflammatory bowel diseases (IBDs), including Crohn's disease and ulcerative colitis. IBD is a chronic inflammatory disorder that causes small and/or large intestines ulceration. According to previous studies, recombinant interleukin (IL)-10 protein and genetically modified bacteria secreting IL-10 ameliorate dextran sulfate sodium (DSS)-induced colitis in mice. IL-19 is a transcriptional activator of IL-10 and can alter the balance of T helper 1 (Th)1/Th2 cells in favor of Th2. In this study, we aimed to investigate whether the expression of the murine IL-19 gene carried by Salmonella choleraesuis (S. choleraesuis) could ameliorate murine IBD. Our results showed that the attenuated S. choleraesuis could carry and express the IL-19 gene-containing plasmid for IBD gene therapy by reducing the mortality and clinical signs in DSS-induced acute colitis mice as compared to the untreated ones. We also found that IL-10 expression was induced in IL-19-treated colitis mice and prevented inflammatory infiltrates and proinflammatory cytokine expression in these mice. We suggest that S. choleraesuis encoding IL-19 provides a new strategy for treating IBD in the future.enSalmonella choleraesuis; dextran sulfate sodium-induced colitis; inflammatory bowel diseases; interleukin-19[SDGs]SDG3journal article10.3390/microorganisms11061530373750322-s2.0-85163842638https://api.elsevier.com/content/abstract/scopus_id/85163842638