Abstract:
Although systemic lupus erythematosus (SLE) is known as the autoimmune disease that triggers inflammation and bone impairment, the mechanisms leading to the decrease in bone regeneration remain inadequately characterized. Patients with SLE have been observed high prevalence in bone loss due to host immune responses that may induce host antimicrobial activities. Here, this study used systemic and local lipopolysaccharide (LPS) administration for mimicking infectious condition in FcγRIIB−/− mice as a lupus murine model. The results showed FcγRIIB lacking FcγRIIB−/− in mice with local and systemic LPS led to decreased cancellous bone volume in their drilled hole region of tibial and mandibular bone compared to WT, FcγRIIB−/−, and WT+LPS groups. Likewise, the data of aniline blue staining in histological analysis showed a decrease of mineralization/collagen ratio in FcγRIIB-deficient activated by local and systemic LPS compared to others. Deleting FcγRIIB with LPS administration increased osteoclast gene expression but decreased osteoblast gene expression indicating the reduction of bone regeneration. Moreover, serum TNF-α, IL-6, and MCP-1 level was high in FcγRIIB−/−+ LPS mice. The induction of proinflammatory cytokines may cause LPS-induced osteoclast formation and a decrease in osteoblasts that have an important role in collagen production. Herein, LPS administration could suppress bone regeneration and collagen accumulation in cancellous bone of mandible and tibia of mice with FcγRIIB deletion by increasing serum proinflammatory cytokines.
