Inflammatory bowel disease (IBD) is caused by chronic inflammation of the gastrointestinal tract. The pathogenesis of IBD remains unclear. The inflammation is associated with activation of T helper (Th) lymphocytes and chronic production of inflammatory cytokines. Ro60 suppresses the expression of tumor necrosis factor α, interleukin (IL)-6, and interferon α by inhibiting Alu transcription; control of Ro60 mRNA expression may thus be therapeutically useful. However, few studies have evaluated the anti-inflammatory activity of Ro60. The Ro60 level is decreased in IBD patients; we thus hypothesized that Ro60 was involved in the development of this autoimmune disease. We subjected mice with dextran sodium sulfate (DSS)-induced colitis to gene therapy using a vector that overexpressed Ro60 threefold. We scored IBD progression by repeatedly weighing the mice. Ro60 ameliorated colitis severity and reduced the levels of tumor necrosis factor α, IL-6, IL-17, IL-8, and vascular endothelial growth factor. Ro60 overexpression decreased the levels of α-smooth muscle actin (a marker of activated myofibroblasts) and type I collagen. The anti-inflammatory and anti-fibrotic activities of Ro60 ameliorated the severity of DSS-induced colitis in mice by repressing inflammation, fibrosis, angiogenesis, and the production of reactive oxygen species.
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