Inhibition of Complement Retards Ankylosing Spondylitis Progression

• DOI: 10.1038/srep34643
• Publication Date: 2016-10-04T11:50:23Z
• Authors: Chaoqun Yang; Peipei Ding; Qingkai Wang; Long Zhang; Xin Zhang; Jianquan Zhao; Enjie Xu; Na Wang; Jianfeng Chen; Guang Yang; Weiguo Hu; Xuhui Zhou
• Keywords: Pathogenesis

Abstract Ankylosing spondylitis (AS) is a chronic axial spondyloarthritis (SpA) resulting in back pain and progressive spinal ankyloses. Currently, there are no effective therapeutics targeting AS largely due to elusive pathogenesis mechanisms, even as potential candidates such HLA-B27 autoantigen have been identified. Herein, we employed proteoglycan (PG)-induced mouse model together with clinical specimens, found that the complement system was substantially activated bone marrow, accompanied by remarkable proportion alteration of neutrophils macrophage marrow spleen, significant increase TGF-β1 serum. The combined treatment bacteria-derived inhibitor Efb-C ( C -terminal e xtracellular f ibrinogen- b inding protein Staphylococcus aureus ) remarkably retarded progression reducing osteoblast differentiation. Furthermore, demonstrated two important modulators involved disease, RANKL, were elevated upon vitro attack and/or osteoclast cells. These findings further unravel activation closely related AS, suggest inhibition may hold great for therapy.