Lactobacillus sakei OK67 ameliorates collagen-induced arthritis in mice by inhibiting NF-κB activation and restoring Th17/Treg cell balance

The anti-inflammatory effects of Th17-inhibiting bacterial strain Lactobacillus sakei OK67 were investigated in DMA/1J mice with collagen II-induced arthritis (CIA). OK67 significantly suppressed IL-6/TGF-beta-induced differentiation of splenic T cells into Th17 cells in vitro. Oral administration of OK67 (1 x 10(9) CFU/mouse) significantly decreased CIA incidence, paw thickness, and clinical index in the paws of mice, as well as myeloperoxidase activity, nitric oxide, and prostaglandin E2 production. OK67 treatment inhibited collagen-induced Th17 cell differentiation and increased collagen-suppressed Treg cell differentiation in bone marrow. OK67 treatment also inhibited TNF-alpha, IL-1 beta, and IL-17 expression in the joint tissues of CIA mice. However, OK67 induced IL-10 expression. Furthermore, treatment with OK67 inhibited collagen-induced activation of NF-kappa B and MAPKs. Additionally, OK67 inhibited NF-kappa B activation in LPS-stimulated peritoneal macrophages. These findings suggest that OK67 may ameliorate inflammatory diseases such as rheumatoid arthritis by restoring the balance of Th17/Treg cells and inhibiting macrophage activation of NF-kappa B and MAPKs. (C) 2015 Elsevier Ltd. All rights reserved.