PBP3 GENE ACTIVATOR

aureus has evolved to express various virulence mechanisms that enhance its survival and ability to evade host immunity. In the setting of implant-associated bone infection, S. aureus can also cause severe disease as an opportunistic pathogen ( Lowy, 1998). Despite its ability to asymptomatically colonize a large percentage of the population, S. Staphylococcus aureus is a ubiquitous organism of the human microbiota colonizing the nares of approximately 30% of individuals ( Kluytmans et al., 1997). aureus cell wall synthesis enzymes are critical for OLCN invasion and osteomyelitis pathogenesis in vivo. Together, these results demonstrate that S. Most notably, transmission electron microscopy (TEM) imaging of infected bone showed that pbp3 was the only gene herein associated with decreased submicron invasion of canaliculi in vivo.

PBP3 GENE ACTIVATOR

Further, peri-implant osteolysis, osteoclast activity, and receptor activator of nuclear factor kappa-B ligand (RANKL) production were decreased following pbp3 deletion. aureus abscess formation in the medullary cavity, while deletion of surface adhesins showed no significant differences. Specifically, deletion of pbp3 and atl decreased septic implant loosening and S. aureus osteomyelitis pathogenesis, while surface adhesins had minimal effects. aureus cell wall synthesis proteins were found to be key modulators of S. Using a murine model for implant-associated osteomyelitis, S. In vitro evaluation in the microfluidic silicon membrane-canalicular array (ОјSiM-CA) showed pbp3, atl, clfA, and sasC deletion reduced nanopore propagation. aureus cell wall synthesis mutants (О”pbp3, О”atl, and О”mreC) and surface adhesin mutants (О”clfA and О”sasC) for nanopore propagation in vitro and osteomyelitis pathogenesis in vivo. Given these findings, we hypothesized that cell wall synthesis machinery and surface adhesins enable durotaxis- and haptotaxis-guided invasion of the OLCN, respectively. aureus surface protein C (SasC), as critical factors for bacterial deformation and propagation through nanopores in vitro, representative of the confined canaliculi in vivo. aureus cell wall transpeptidase, penicillin binding protein 4 (PBP4), and surface adhesin, S. Staphylococcus aureus invasion of the osteocyte lacuno-canalicular network (OLCN) is a novel mechanism of bacterial persistence and immune evasion in chronic osteomyelitis.

Pbp3 gene