AIM To explore the mechanism by which micro RNA-155(miR-155) regulates the pathogenesis of experimental colitis.METHODS A luciferase assay was performed to confirm the binding of miR-155 to the SHIP-1 3’-UTR. MiR-155 mimics, negative controls and SHIP-1 expression/knockdown vectors were established and then utilized in gain-and loss-of-function studies performed in raw264.7 cells and primary bone marrow-derived macrophages (BMDMs). Thereafter, dextran sulfate sodium(DSS)-induced colitis mouse model with or without antagomiR-155 treatment was established, and the levels of miR-155 and SHIP-1, as well as the pro-inflammatory capabilities, were measured by western blot, quantitative polymerase chain reaction, and immunohistochemistry.RESULTS MiR-155 directly bound to the 3’-UTR of SHIP-1 mRNA and induced a significant decrease in SHIP-1 expression in both raw264.7 cells and primary BMDMs. MiR-155 markedly promoted cell proliferation and proinflammatory secretions including IL-6, TNF-α, IL-1β, and IFN-γ, whereas these effects could be reversed by the restoration of SHIP-1 expression. In vivo studies showed that antagomiR-155 administration could alleviate DSS-induced intestinal inflammation in Balb/c mice. Moreover, significantly increased SHIP-1 expression, as well as decreased Akt activation and inflammatory response, were observed in the antagomiR-155-treated mice.CONCLUSION MiR-155 promotes experimental colitis by repressing SHIP-1 expression. Thus, the inhibition of miR-155 might be a promising strategy for therapy. AIM To explore the mechanism by which micro RNA-155 (miR-155) regulates the pathogenesis of experimental colitis. METHODS A luciferase assay was performed to confirm the binding of miR-155 to the SHIP-1 3’-UTR. mimics, negative controls and SHIP-1 expression / knockdown vectors were established and then utilized in gain-and loss-of-function studies performed in raw 264.7 cells and primary bone marrow-derived macrophages (BMDMs). DSS) -induced colitis mouse model with or without antagomi R-155 treatment was established, and the levels of miR-155 and SHIP-1, as well as the pro-inflammatory capabilities, were measured by western blot, quantitative polymerase chain reaction, and immunohistochemistry. RESULTS MiR-155 directly bound to the 3’-UTR of SHIP-1 mRNA and induced a significant decrease in SHIP-1 expression in both raw 264.7 cells and primary BMDMs. MiR-155 markedly promoted cell proliferation and proinflammatory secretions including IL-6, TNF-α, I L-1β, and IFN-γ, but these effects could be reversed by the restoration of SHIP-1 expression. In vivo studies showed that antagomi R-155 administration could alleviate DSS-induced intestinal inflammation in Balb / c mice. SHIP-1 expression, as well as decreased Akt activation and inflammatory response, were observed in the antagomi R-155-treated mice. CONCLUSION: MiR-155 is available as colitis by repressing SHIP-1 expression. Thus, the inhibition of miR- a promising strategy for therapy.