AIM: This study aimed to investigate the anti-inflammatory mechanism of IL-25 mediated mesenchymal stem cells (MSC) treatment for inflammatory bowel disease (IBD) in a DSS-induced rat colitis model. METHODS: Rats with DSS-induced colitis were divided into control and treatment groups: normal control group (rats fed with water), DSS group (rats fed with DSS solution), MSC group (DSS-treated rats injected intravenously with GFP-MSCs), IL-25-MSC group (DSS-treated rats injected intravenously with IL-25 primed GFP-MSCs), and mesalazine group (DSS-treated rats fed with mesalazine). RESULTS: In IL-25-MSC group, therapeutic efficacy (clinical symptoms) was better than in MSC group, but comparable to mesalazine group. In IL-25-MSC group and mesalazine group, fewer infiltrating inflammatory cells and lower pathological score were observed in the intestine. The FOXP3+ cells and IL-4+ cells decreased, but IL-17A+ cells and IFN-γ+ cells increased in the peripheral blood and colonic mucosa after DSS induced colitis, and these phenomena were reversed by MSC or mesalazine treatment. IL-17A+ cells reduced and FOXP3+ cells increased in IL-25-MSC group as compared with MSC group. The expressions of Ki67 and LGR5 were significantly elevated in MSC treatment groups as compared with normal control group, DSS group, and mesalazine group. Definite GFP positive cells were not observed in the intestine of MSC-treated rats. CONCLUSION: IL-25 primed MSCs exert improved therapeutic effects on the intestinal inflammation of IBD rats which may be related to the inhibition of Th17 immune response and induction of T Regulatory cell phenotype. Thus, IL-25 may be an attractive candidate for MSC-based therapy of IBD.
AIM: This study aimed to investigate the anti-inflammatory mechanism of IL-25 mediated mesenchymal stem cells (MSC) treatment for inflammatory bowel disease (IBD) in a DSS-induced ratcolitis model. METHODS:Rats with DSS-induced colitis were divided into control and treatment groups: normal control group (rats fed with water), DSS group (rats fed with DSS solution), MSC group (DSS-treated rats injected intravenously with GFP-MSCs), IL-25-MSC group (DSS-treated rats injected intravenously with IL-25 primed GFP-MSCs), and mesalazine group (DSS-treated rats fed with mesalazine). RESULTS: In IL-25-MSC group, therapeutic efficacy (clinical symptoms) was better than in MSC group, but comparable to mesalazine group. In IL-25-MSC group and mesalazine group, fewer infiltrating inflammatory cells and lower pathological score were observed in the intestine. The FOXP3+ cells and IL-4+ cells decreased, but IL-17A+ cells and IFN-γ+ cells increased in the peripheral blood and colonic mucosa after DSS induced colitis, and these phenomena were reversed by MSC or mesalazine treatment. IL-17A+ cells reduced and FOXP3+ cells increased in IL-25-MSC group as compared with MSC group. The expressions of Ki67 and LGR5 were significantly elevated in MSC treatment groups as compared with normal control group, DSS group, and mesalazine group. Definite GFP positive cells were not observed in the intestine of MSC-treated rats. CONCLUSION:IL-25 primed MSCs exert improved therapeutic effects on the intestinal inflammation of IBD rats which may be related to the inhibition of Th17 immune response and induction of T Regulatory cell phenotype. Thus, IL-25 may be an attractive candidate for MSC-based therapy of IBD.
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