Determination of the Patho-Mechanisms Associated with Staphylococcus aureus Osteomyelitis

Introduction: Osteomyelitis is an inflammatory bone disease caused by an infecting microorganism. Staphylococcus aureus (SA) is responsible for up to 75% of clinical cases. Recent studies have demonstrated that bone cell invasion contributes to the development of infection. Little work has been done to investigate whether there are strain-dependent differences in regard to SA's ability to alter osteoblast physiology. We hypothesized that SA may elicit strain-dependent differences in its ability to induce inflammatory bone pathology.

Materials and Methods: MC3T3-E1 osteoblast cells were used. Cells were seeded at 100,000 cells per well in 12-well cell culture plates and grown until 80% confluent for all apoptosis and cytokine assays. Cells were inoculated with either SA strain ST 398 (goat isolate), USA 300 (human isolate), or Cowan I (laboratory isolate; M.O.I 250:1). Infected cells were subjected to either transmission electron microscopy, apoptosis staining, or inflammatory cytokine (interleukin-6; IL-6) analysis.

Results: Osteoblasts infected by the Cowan I strain showed bacteria with distorted shape apparently limited to the cell wall of the osteoblasts. Both USA 300 and ST 398 infected osteoblasts showed SA had established intracellular infection. ST 398 and USA 300 induced a greater degree of late-stage apoptosis and an increased bone inflammatory response as compared with Cowan I.

Discussion/Conclusion: Different strains of SA vary in their ability to alter osteoblast physiology and induce osteoblast-related physiologic changes. Future work may allow additional characterization of these physiologic changes offering the potential to arrest bone infection at the bone formation stage, ultimately leading to therapeutic potential.

Acknowledgements: Funding for this study was provided by the Centre of Excellence in Livestock Diseases and Human Health, College of Veterinary Medicine, University of Tennessee.

Publication History

Article published online:
26 October 2022