English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Severe  Staphylococcus aureus  ( S .  aureus ) infections pose an immense threat to population health and constitute a great burden for the health care worldwide.  Inter alia ,  S .  aureus  septic arthritis is a disease with high mortality and morbidity caused by destruction of the infected joints and systemic bone loss, osteoporosis. Toll-Like receptors (TLRs) are innate immune cell receptors recognizing a variety of microbial molecules and structures.  S .  aureus  recognition via TLR2 initiates a signaling cascade resulting in production of various cytokines, but the mechanisms by which  S .  aureus  causes rapid and excessive bone loss are still unclear. We, therefore, investigated how  S .  aureus  regulates periosteal/endosteal osteoclast formation and bone resorption.  S .  aureus  stimulation of neonatal mouse parietal bone induced  ex vivo  bone resorption and osteoclastic gene expression. This effect was associated with increased mRNA and protein expression of receptor activator of NF-kB ligand (RANKL) without significant change in osteoprotegerin (OPG) expression. Bone resorption induced by  S .  aureus  was abolished by OPG.  S .  aureus  increased the expression of osteoclastogenic cytokines and prostaglandins in the parietal bones but the stimulatory effect of  S .  aureus  on bone resorption and  Tnfsf11  mRNA expression was independent of these cytokines and prostaglandins. Stimulation of isolated periosteal osteoblasts with  S .  aureus  also resulted in increased expression of  Tnfsf11  mRNA, an effect lost in osteoblasts from  Tlr2  knockout mice.  S .  aureus  stimulated osteoclastogenesis in isolated periosteal cells without affecting RANKL-stimulated resorption. In contrast,  S .  aureus  inhibited RANKL-induced osteoclast formation in bone marrow macrophages. These data show that  S .  aureus  enhances bone resorption and periosteal osteoclast formation by increasing osteoblast RANKL production through TLR2. Our study indicates the importance of using different  in vitro  approaches for studies of how  S .  aureus  regulates osteoclastogenesis to obtain better understanding of the complex mechanisms of  S .  aureus  induced bone destruction  in vivo .

Toll-Like Receptor 2 Stimulation of Osteoblasts Mediates Staphylococcus Aureus Induced Bone Resorption and Osteoclastogenesis through Enhanced RANKL