Inhibition of Wnt11 impairs the osteogenesis and aggravates the inflammatory response of human mesenchymal stem cells under LPS-induced inflammatory condition.

In infectious bone defect, osteogenesis is very particularly important for treating. Currently, mesenchymal stem cells (MSCs) become a promising treatment protocol in clinical practice. In infectious environment, lipopolysaccharide (LPS) not only affects the osteogenic differentiation of MSCs, but also incurs inflammatory reaction from the host or cells and prompts the secretion of inflammatory cytokines.

Staphylococcus Aureus Induces Osteoclastogenesis via the NF-κB Signaling Pathway.

BACKGROUND Osteomyelitis is one of the refractory diseases encountered in orthopedics, while Staphylococcus aureus (S. aureus) is the most common causative organism in osteomyelitis. However, the precise mechanisms underlying the bone loss caused by S.

Staphylococcus aureus Protein A induces osteoclastogenesis via the NF‑κB signaling pathway.

Staphylococcus aureus (S. aureus) is the most common organism causing osteomyelitis, and Staphylococcus aureus protein A (SpA) is an important virulence factor anchored in its cell wall. However, the precise mechanisms underlying the bone loss caused by SpA have not been well understood.