Protein A effect on alternative pathway complement activation and opsonization of Staphylococcus aureus

Area of Science:

• Immunology
• Microbiology
• Bacteriology

Background:

• Staphylococcus aureus produces protein A, a cell wall component.
• Protein A's role in immune evasion is not fully understood.
• The alternative complement pathway is crucial for innate immunity.

Purpose of the Study:

• To investigate the impact of Staphylococcus aureus protein A on alternative pathway complement activation.
• To determine if protein A affects bacterial opsonization and phagocytosis.
• To elucidate the mechanism by which protein A influences host-pathogen interactions.

Main Methods:

• Comparison of complement activation and opsonization by Staphylococcus aureus strains with varying protein A content.
• Assessment of phagocytosis by human polymorphonuclear leukocytes after opsonization in chelated serum.
• Analysis of complement activation and opsonization in normal human serum.

Main Results:

• "Protein A-poor" S. aureus strains showed significantly higher alternative pathway complement activation compared to "protein A-rich" strains.
• Protein A-poor strains were more effectively phagocytized by human leukocytes after opsonization in chelated serum.
• No significant differences were observed in normal serum, suggesting protein A interferes with the alternative pathway specifically.

Conclusions:

• Cell wall-bound protein A inhibits alternative pathway complement activation by Staphylococcus aureus.
• This inhibition leads to decreased opsonization and phagocytosis of S. aureus, particularly when the classical complement pathway is absent.
• Protein A may shield complement-activating sites on the bacterial cell wall, facilitating immune evasion.