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Vaccinia Virus Complement Control Protein Ameliorates Collagen‐Induced Arthritic Mice
Author(s) -
JHA PURUSHOTTAM,
SMITH SCOTT A.,
JUSTUS DAVID E.,
KOTWAL GIRISH J.
Publication year - 2005
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1352.004
Subject(s) - vaccinia , complement control protein , complement (music) , virus , complement system , virology , chemistry , immunology , medicine , antibody , classical complement pathway , recombinant dna , phenotype , biochemistry , complementation , gene
The main objective of this study was to investigate the therapeutic efficiency of recombinant vaccinia virus complement control protein (rVCP) on collagen‐induced arthritis (CIA) in DBA‐1/J mice. Arthritis was induced in DBA‐1J mice by injecting bovine collagen emulsified in complete Freunds adjuvant. We used rVCP to block complement activation and investigated its effect on different aspects of CIA including osteoclast formation and bone destruction. The osteoclast‐like cells were detected using immunohistochemistry. Joint destruction was studied using X‐ray of the intact knee joints. Cartilage destruction was monitored by staining the paraffin sections with toluidine blue. ELISA was used to measure the cytokine levels in the serum. Blocking complement activation in DBA/1J arthritic mice with rVCP resulted in significant inhibition of the clinical progression of the disease and reduction in joint destruction as revealed by X‐ray analysis and toluidine blue staining of the joint sections. Inhibition of complement reduced the production of proinflammatory cytokines and the number of osteoclast‐like cells in arthritic joints. In conclusion, blocking of complement in CIA by rVCP inhibits the inflammation and the formation of osteoclast‐like cells and reduces cartilage destruction.