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Serum complement factor I decreases Staphylococcus aureus phagocytosis.

Kenji M Cunnion1, E Stephen Buescher, Pamela S Hair

  • 1Department of Pediatrics, Eastern Virginia Medical School and Children's Hospital of The King's Daughters, Norfolk, USA. cunniok@chkd.org

The Journal of Laboratory and Clinical Medicine
|October 26, 2005
PubMed
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Staphylococcus aureus evades immune defenses by manipulating complement factor I to cleave C3b, reducing phagocytosis. Inhibiting this cleavage may offer a new therapeutic strategy against S. aureus infections.

Area of Science:

  • Immunology
  • Microbiology
  • Biochemistry

Background:

  • Complement-mediated opsonization is crucial for host defense against Staphylococcus aureus.
  • Complement component C3b and its regulator CD35 are key players in S. aureus opsonophagocytosis.
  • Factor I cleaves C3b on the S. aureus surface, a process investigated for its physiological impact.

Purpose of the Study:

  • To determine if factor I-mediated cleavage of S. aureus-bound C3b affects neutrophil-mediated phagocytosis.
  • To investigate the role of factor I in bacterial evasion of complement-dependent immune responses.

Main Methods:

  • Antibodies against factor I were used to inhibit C3b cleavage.
  • Factor I was applied to C3b-coated S. aureus to assess its effects.
  • Quantification of C3b cleavage products (iC3b) and C3 fragments on the bacterial surface.

Related Experiment Videos

  • Measurement of bacterial phagocytosis by neutrophils.
  • Assessment of C3 fragment shedding from the bacterial surface.

    • Main Results:

    • Inhibition of factor I activity increased S. aureus phagocytosis by over 100%.
    • Factor I treatment enhanced iC3b generation by 75% and C3 fragment shedding by 43%.
    • Factor I treatment decreased total C3 fragments on S. aureus by 58% and reduced phagocytosis by 40%.
    • Factor I's effects on C3b cleavage and phagocytosis were independent of factor H.

    Conclusions:

    • Staphylococcus aureus appears to exploit factor I-mediated C3b cleavage to evade complement-dependent opsonophagocytosis.
    • This bacterial evasion mechanism is crucial for survival and pathogenesis.
    • Targeting factor I-mediated C3b cleavage presents a potential therapeutic strategy to enhance bacterial clearance.