Inhibition of Complement Retards Ankylosing Spondylitis Progression.
Inhibition of Complement Retards Ankylosing Spondylitis Progression.
复制标题
抑制补体可延缓强直性脊柱炎的进展。
DOI：
10.1038/srep34643
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发表时间：
2016-10-04
影响因子：
4.6
通讯作者：
Zhou X
中科院分区：
文献类型：
--
作者：
Yang C;Ding P;Wang Q;Zhang L;Zhang X;Zhao J;Xu E;Wang N;Chen J;Yang G;Hu W;Zhou X
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 as HLA-B27 autoantigen have been identified. Herein, we employed a proteoglycan (PG)-induced AS mouse model together with clinical specimens, and found that the complement system was substantially activated in the spinal bone marrow, accompanied by a remarkable proportion alteration of neutrophils and macrophage in bone marrow and spleen, and by the significant increase of TGF-β1 in serum. The combined treatment with a bacteria-derived complement inhibitor Efb-C (C-terminal of extracellular fibrinogen-binding protein of Staphylococcus aureus) remarkably retarded the progression of mouse AS by reducing osteoblast differentiation. Furthermore, we demonstrated that two important modulators involved in AS disease, TGF-β1 and RANKL, were elevated upon in vitro complement attack in osteoblast and/or osteoclast cells. These findings further unravel that complement activation is closely related with the pathogenesis of AS, and suggest that complement inhibition may hold great potential for AS therapy.
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影响因子：
--
作者：
Haroon, Nigil;Inman, Robert D.;Learch, Thomas J.;Weisman, Michael H.;Lee, MinJae;Rahbar, Mohammad H.;Ward, Michael M.;Reveille, John D.;Gensler, Lianne S.
通讯作者：
Gensler, Lianne S.
影响因子：
2.6
作者：
Gao, Ya-ping;Dong, Jie;Yang, Guang
通讯作者：
Yang, Guang
影响因子：
--
作者：
Inman, Robert D.;Davis, John C., Jr.;Braun, Juergen
通讯作者：
Braun, Juergen
影响因子：
5.7
作者：
Acosta, JA;Benzaquen, LR;Halperin, JA
通讯作者：
Halperin, JA
影响因子：
1.5
作者：
Ebringer, Alan;Rashid, Taha;Fielder, Mark
通讯作者：
Fielder, Mark