Intracellular Dynamics of Staphylococcus aureus Infections
Summary
Staphylococcus aureus is adept at invading a wide range of host cells, including professional phagocytes (macrophages and neutrophils) and non-professional phagocytes (endothelial, epithelial and osteoblast cells). Once internalised, it employs diverse strategies to survive and replicate: escaping from early phagosomes into the cytoplasm, subverting autophagy pathways to prevent phagolysosomal maturation, adopting small colony variant phenotypes to persist in a quiescent state, and modulating host‐cell death programmes. Intracellular survival affords protection from antibiotic exposure and immune clearance, facilitates dissemination via mobile immune cells, and contributes to chronic or relapsing infections, particularly in implant‐associated and endovascular settings. Key virulence regulators such as the agr quorum-sensing system and alternative sigma factors orchestrate the expression of toxins (for example alpha-toxin) and surface proteins that mediate cellular entry, intracellular trafficking and immune evasion. Understanding these intracellular niches reveals critical vulnerabilities for novel therapeutic approaches that target both bacterial and host pathways to eradicate hidden reservoirs and prevent systemic spread.
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Intracellular Dynamics of Staphylococcus aureus Infections publication trend
The graph below shows the total number of articles in intracellular dynamics of staphylococcus aureus infections across all publications each year (not limited to Nature Index journals).
Technical terms
Phagosome: A membrane-bound vesicle formed around ingested pathogens within phagocytic cells.
Phagolysosome: A matured phagosome fused with lysosomes, containing degradative enzymes and acidic pH.
Autophagy: A cellular self-degradation process in which cytoplasmic components are sequestered into double-membrane vesicles for lysosomal breakdown.
Antibody-antibiotic conjugate (AAC): A targeted therapeutic in which an antibody directs an antibiotic to specific bacterial cells and releases the drug intracellularly.
Small colony variant (SCV): A slow-growing bacterial phenotype characterised by reduced metabolism and enhanced intracellular persistence.
References
- Antibody-antibiotic conjugate targeted therapy for orthopedic implant-associated intracellular S. aureus infections. Journal of Advanced Research (2023).
- Antimicrobial Mechanisms of Macrophages and the Immune Evasion Strategies of Staphylococcus aureus. Pathogens (2015).
- Inability to sustain intraphagolysosomal killing of Staphylococcus aureus predisposes to bacterial persistence in macrophages. Cellular Microbiology (2015).
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