Staphylococcus aureus Protein A induces osteoclastogenesis via the NFκB signaling pathway.
Mol Med Rep
; 16(5): 6020-6028, 2017 Nov.
Article
en En
| MEDLINE
| ID: mdl-28849198
ABSTRACT
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. The present study aimed to investigate the effect of SpA on osteoclast differentiation, and the probable mechanism was investigated. Raw264.7 cells were treated with SpA in the absence or presence of receptoractivated (NF)κB ligand for 5 days, and morphological and biochemical assays were used to assess osteoclastogenesis and explore the underlying mechanisms. Data demonstrated that SpA induced osteoclast differentiation and promoted bone resorption in a dosedependent manner in the absence or presence of RANKL. In addition, the expression of osteoclastspecific genes, such as the tartrate resistant acid phosphatase, matrix metalloproteinase9, cathepsin K, calcitonin receptors and d2 isoform of the vacuolar ATPase Vo domain, were enhanced by SpA. Furthermore, the SpAinduced osteoclast differentiation was associated with the degradation of inhibitor of κBα, phosphorylation of NFκB p65 and increased expression of nuclear factor of activated Tcells. However, by treatment with JSH23, an NFκB inhibitor, the formation of osteoclastlike cells and resorption pits was significantly reduced, and the expression of osteoclastspecific genes was also inhibited. Collectively, in the present study SpA induced osteoclast differentiation, promoted bone resorption, and the NFκB signaling pathway was involved in this process.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Osteoclastos
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Osteogénesis
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Proteína Estafilocócica A
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Transducción de Señal
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FN-kappa B
Límite:
Animals
Idioma:
En
Revista:
Mol Med Rep
Año:
2017
Tipo del documento:
Article