Immune Evasion Strategies in Staphylococcus aureus Infections

Staphylococcus aureus employs a multifaceted arsenal of mechanisms to circumvent host defences and establish persistent infections across diverse tissues. Central to its success is the secretion of surface-associated and secreted proteins that bind and inactivate key components of the complement cascade, thereby preventing opsonisation and membrane attack complex formation. The bacterium further remodels its cell wall in response to serum factors, thickening peptidoglycan layers to shield bound antibodies and complement fragments from recognition by phagocytes. Biofilm formation on implant surfaces or within bone tissue provides a physical barrier to immune cell infiltration and antibiotic penetration, while specialised toxins and immune modulators interfere with neutrophil chemotaxis, degranulation and the formation of neutrophil extracellular traps (NETs). Enzymatic production of adenosine by a surface-anchored nucleotidase dampens local inflammatory signalling, skewing host responses towards immune tolerance. Molecular mimicry of host regulators, such as recruitment of plasminogen and factor H to the bacterial surface, accelerates degradation of complement components in the fluid phase, further blunting innate defences. Collectively, these strategies allow S. aureus to adapt to diverse host niches, evade clearance and resist therapeutic interventions.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Immune Evasion Strategies in Staphylococcus aureus Infections publication trend

The graph below shows the total number of articles in immune evasion strategies in staphylococcus aureus infections across all publications each year (not limited to Nature Index journals).

Technical terms

Opsonin: a molecule, such as an antibody or complement fragment, that marks pathogens for phagocytic uptake.

Opsonophagocytosis: the process by which opsonised microbes are ingested and destroyed by phagocytic cells.

Complement system: a cascade of plasma proteins that amplifies inflammation, opsonisation and lytic destruction of pathogens.

Neutrophil extracellular traps (NETs): networks of DNA and antimicrobial proteins expelled by neutrophils to immobilise and kill bacteria.

Host-directed therapy (HDT): an intervention targeting host cell pathways to bolster immune defence or restrict pathogen survival without directly targeting the microbe.

References

1. Targeting host deoxycytidine kinase mitigates Staphylococcus aureus abscess formation. eLife (2024).
2. Host-induced cell wall remodeling impairs opsonophagocytosis of Staphylococcus aureus by neutrophils. mBio (2024).
3. Dalbavancin Boosts the Ability of Neutrophils to Fight Methicillin-Resistant Staphylococcus aureus. International Journal of Molecular Sciences (2023).
4. Enzymatic properties of Staphylococcus aureus adenosine synthase (AdsA). BMC Molecular and Cell Biology (2011).
5. The Staphylococcus aureus Protein Sbi Acts as a Complement Inhibitor and Forms a Tripartite Complex with Host Complement Factor H and C3b. PLOS Pathogens (2008).
6. Staphylococcus aureus Proteins Sbi and Efb Recruit Human Plasmin to Degrade Complement C3 and C3b. PLOS ONE (2012).
7. A New Staphylococcal Anti-Inflammatory Protein That Antagonizes the Formyl Peptide Receptor-Like 1. The Journal of Immunology (2006).
8. Evasion of Neutrophil Killing by Staphylococcus aureus. Pathogens (2016).