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Updated: Sep 9, 2025
Development and Assessment of Intracellular Infection Models for Staphylococcus aureus
Published on: January 17, 2025
Intracellular survival of Staphylococcus aureus in macrophages during osteomyelitis
William A Lathram1, Christopher D Radka1
1Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky, Lexington, KY, USA.
Abstract:
Staphylococcus aureus, traditionally viewed as an extracellular pathogen, is increasingly recognized for its ability to persist intracellularly, particularly within macrophages. This intracellular lifestyle is central to osteomyelitis, a chronic bone infection characterized by persistent inflammation, bone destruction, and impaired repair. Within bone, S. aureus exploits macrophage plasticity by driving a shift from pro-inflammatory, bactericidal M1-like states to anti-inflammatory, tissue-reparative M2-like phenotypes. This polarization suppresses immune clearance and promotes an environment conducive to bacterial survival and dissemination. Additional strategies - including biofilm formation, small colony variants, and inhibition of phagolysosomal killing - further enhance persistence and immune evasion. While these mechanisms are well studied in extracellular infections, their role in intracellular survival is increasingly evident. This review synthesizes emerging insights into how S. aureus manipulates macrophage function to establish chronic bone infection and highlights therapeutic opportunities targeting macrophage polarization to improve immune-mediated clearance and bone repair in osteomyelitis.
Insights
Staphylococcus aureus can survive inside macrophages, promoting chronic bone infections like osteomyelitis by altering immune cells. Targeting this intracellular behavior offers new treatment strategies for bone repair and bacterial clearance.
Area of Science:
- Microbiology
- Immunology
- Bone Biology
Background:
- Staphylococcus aureus is increasingly recognized for its intracellular survival within macrophages, a key factor in chronic osteomyelitis.
- This intracellular persistence contributes to persistent inflammation, bone destruction, and impaired healing characteristic of osteomyelitis.
Purpose of the Study:
- To review the mechanisms by which Staphylococcus aureus manipulates macrophage function for intracellular survival in osteomyelitis.
- To highlight therapeutic strategies targeting macrophage polarization for improved treatment outcomes.
Main Methods:
- This review synthesizes current literature on Staphylococcus aureus's intracellular lifestyle and its impact on macrophage phenotype.
- Analysis of bacterial strategies such as biofilm formation, small colony variants, and inhibition of phagolysosomal killing in the context of intracellular infection.
Main Results:
- Staphylococcus aureus drives macrophage polarization from M1 (pro-inflammatory) to M2 (anti-inflammatory, tissue-reparative) phenotypes within bone.
- This polarization suppresses immune clearance, promotes bacterial survival, and contributes to the chronic nature of osteomyelitis.
- Bacterial strategies like biofilm formation and immune evasion are crucial for intracellular persistence.
Conclusions:
- Staphylococcus aureus's intracellular lifestyle and manipulation of macrophage polarization are critical for establishing chronic osteomyelitis.
- Targeting macrophage polarization presents a promising therapeutic avenue to enhance bacterial clearance and promote bone repair in osteomyelitis.
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