Osteoarticular Brucellosis: inflammation, matrix metalloproteinases and induction of osteoclastogensis.

M. VICTORIA DELPINO

Buenos Aires, Argentina

Congreso; 1º Congreso Franco-Argentino de Inmunología (FAIC) y LVIII Reunión Anual de la Sociedad Argentina de Inmunología.; 2010

Resumen de la Conferencia. Osteoarticular complications are common in human brucellosis, but the pathogenic mechanisms involved are largely unknown. Brucella can infect and survive within human osteoblasts and this infection elicits the secretion of chemokines (IL-8 and MCP-1, attractants for neutrophils and monocytes, respectively) that might be involved in the osteoarticular manifestations of brucellosis. The recruitment of phagocytes may enhance the immune response since these cells can be activated within the infection focus to secrete additional inflammatory mediators. In particular, macrophages in inflamed tissues can differentiate not only to osteoclasts (the only cells known so far to be able to degrade bone), but they also appear to accelerate bone resorption through the production of proinflammatory cytokines and matrix metalloproteinases. B. abortus infection induces MMP-2 secretion by osteoblasts and MMP-9 secretion by monocytes and B. abortus lipoproteins are responsible for MMP-9 induction by stimulating the secretion of TNF-a via TLR-2. On the other hand, monocytes in inflamed tissues can also accelerate bone resorption by differentiate to osteoclast, in a way that involved, B. abortus lipoproteins throught MYD88 and TLR-2 pathway and dependent on TNF-a production. These results suggest that proinflammatory responses elicited by B. abortus which induce MMPs and the increase of osteoclast cells may be involved in the tissue damage observed in osteoarticular brucellosis