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. 2017 Feb 20;8:256. doi: 10.3389/fmicb.2017.00256

FIGURE 1.

FIGURE 1

Bone damage induced by soluble mediators secreted by resident and infiltrating cells upon infection with Brucella abortus. OSTEOBLAST: B. abortus infection of osteoblast induces RANKL, MMP-2, GM-CSF, and chemokines (IL-8 and MCP-1) expression; induces apoptosis, and inhibits osteoblast differentiation. Chemokines attract monocytes and neutrophils to the site of infection, and these cells secrete MMP-9. TNF-α secreted by B. abortus-infected monocytes inhibits differentiation and induces apoptosis and RANKL expression in osteoblasts. It is the main cytokine involved in the secretion of MMP-9 by monocytes. OSTEOCYTE: B. abortus infection induces MMP-2, RANKL proinflamatory cytokines, and KC secretion by osteocytes. TNF-α and RANKL from B. abortus-infected osteocytes induce osteoclastogenesis. B. abortus infection inhibits the expression of Cx43, but does not modify integrins expression. In contrast, supernatants from B. abortus infected macrophages inhibit Cx43 and integrins inducing osteocyte apoptosis. SYNOVIAL FIBROBLAST: B. abortus infection induces MMP-2 and RANKL expression, and inhibits synoviocyte apoptosis through the upregulation of anti-apoptotic factors (cIAP-2, clusterin, livin, and P21/CIP/CDNK1A) and the reduction in the expression of proteins involved in apoptosis (P-p53(S15) and TNFRI/TNFRSF1A). IMMUNE CELLS AND OSTEOARTICULAR BRUCELLOSIS. Supernatants from B. abortus-infected macrophages induce osteoclastogenesis via TNF-α induction. T cells secrete IL-17 in response to supernatants from B. abortus-infected macrophages, which induce osteoclastogenesis via TNF-α secreted by osteoclast precursors. B. abortus-infected B cells secrete RANKL that induce osteoclastogenesis. L-OMP19. Brucella lipoproteins mimic responses mediated by B. abortus infection in neutrophils, monocytes and synovial fibroblasts and these responses require TLR2.