Rational design and molecular docking-guided screening of high-affinity β-glucosidase affibodies for application in a lateral flow immunoassay platform.

Staphylococcus aureus osteomyelitis drives progressive bone destruction through dysregulated osteoblast-osteoclast crosstalk, yet the role of exosome-mediated circular RNA (circRNA) communication in this process remains poorly understood. This study aimed to determine whether exosomal circRNAs derived from S. aureus-infected osteoblasts orchestrate osteoclast-mediated bone resorption. Exosomes were isolated from hFOB1.19 osteoblasts with or without S. aureus infection, characterized by transmission electron microscopy, nanoparticle tracking analysis, and Western blotting, and their circRNA profiles were screened by RNA sequencing. A murine femoral osteomyelitis model was established via intramedullary S. aureus inoculation followed by tail-vein exosome injection, with bone microarchitecture and osteoclastogenesis assessed by micro-CT, histology, TRAP/ALP staining, qPCR, and Western blotting. The circ_0001843/miR-369-5p/TAFA5 axis was validated by dual-luciferase reporter assays. S. aureus infection markedly upregulated exosomal circ_0001843. In vivo, exosomes from infected osteoblasts aggravated bone destruction, evidenced by decreased BV/TV, increased trabecular separation, enhanced osteoclast activity, and suppressed osteogenic markers. In vitro, circ_0001843 knockdown attenuated RANKL-induced osteoclast differentiation while promoting osteoblast proliferation and mineralization; these protective effects were reversed by exosomes from infected osteoblasts or miR-369-5p inhibition. Mechanistically, circ_0001843 sponged miR-369-5p to derepress TAFA5, thereby disrupting bone remodeling homeostasis. These findings identify exosomal circ_0001843 as a novel mediator of infection-induced bone loss via the miR-369-5p/TAFA5 axis, highlighting a potential therapeutic target for osteomyelitis-associated bone destruction.