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rFSAV promotes Staphylococcus aureus-infected bone defect healing via IL-13- mediated M2 macrophage polarization
Yanhao Zhang1, Feng Yang2, Dong Sun3
1National Engineering Research Center of Immunological Products, Department of Microbiology and Biochemical Pharmacy, College of Pharmacy, Third Military Medical University, Chongqing 400038, China.
Abstract:
Staphylococcus aureus (S. aureus) contamination commonly occurs in orthopedic internal fixation operations, leading to a delayed healing of the defected bone tissue. However, antibiotic treatments are ineffective in dealing with S. aureus bone infections due to the rise in multiple antimicrobial resistances. Here, we reported the protective effects of a recombinant five-antigen S. aureus vaccine (rFSAV) in an S. aureus infected bone defect model. In this study, we found the number of M2 macrophages markedly increased in the defect site and played a critical role in the healing of defected bone mediated by rFSAV. Mechanistically, rFSAV mediated increased level of IL-13 in bone defect site predominant M2 macrophage polarization. In summary, our study reveals a key role of M2 macrophage polarization in the bone regeneration process in S. aureus infection induced bone defect, which provide a promising application of rFSAV for the treatment of bone infection for orthopedic applications.
Insights
A new recombinant five-antigen Staphylococcus aureus (S. aureus) vaccine (rFSAV) promotes bone healing. The vaccine increases M2 macrophages and IL-13 levels, crucial for repairing S. aureus-infected bone defects in orthopedic surgery.
Area of Science:
- Orthopedic surgery
- Infectious disease
- Immunology
Background:
- Staphylococcus aureus infections complicate orthopedic internal fixation, delaying bone healing.
- Antimicrobial resistance limits the efficacy of traditional antibiotic treatments for S. aureus bone infections.
Purpose of the Study:
- To evaluate the protective effects of a recombinant five-antigen S. aureus vaccine (rFSAV) in a murine model of S. aureus-infected bone defects.
- To elucidate the mechanisms underlying rFSAV-mediated bone repair.
Main Methods:
- Establishment of an S. aureus-infected bone defect model in mice.
- Administration of rFSAV to assess its efficacy in promoting bone healing.
- Analysis of immune cell populations, specifically M2 macrophages, and cytokine levels (IL-13) at the defect site.
Main Results:
- rFSAV treatment significantly enhanced bone defect healing in the presence of S. aureus infection.
- A marked increase in M2 macrophages was observed at the bone defect site following rFSAV administration.
- rFSAV mediated increased IL-13 levels, correlating with M2 macrophage polarization.
Conclusions:
- M2 macrophage polarization plays a critical role in bone regeneration during S. aureus infection.
- rFSAV demonstrates promising therapeutic potential for treating orthopedic bone infections by modulating the immune response and promoting healing.
