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Staphylococcal complement inhibitor: structure and active sites.

Suzan H M Rooijakkers1, Fin J Milder, Bart W Bardoel

  • 1Medical Microbiology, University Medical Center Utrecht, Heidelberglaan 100, Utrecht, The Netherlands. s.h.m.rooijakkers@umcutrecht.nl

Journal of Immunology (Baltimore, Md. : 1950)
|August 22, 2007
PubMed
Summary
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Staphylococcal complement inhibitor (SCIN) blocks key immune responses. Identifying its active site reveals an 18-residue segment essential for inhibiting complement pathways and inflammation, paving the way for new therapies.

Area of Science:

  • Immunology
  • Structural Biology
  • Microbial Pathogenesis

Background:

  • Staphylococcus aureus evades host immunity using staphylococcal complement inhibitor (SCIN).
  • SCIN targets central complement convertases, inhibiting opsonization, phagocytosis, and inflammatory mediator production.
  • Understanding SCIN's mechanism is crucial for developing anti-inflammatory therapies.

Purpose of the Study:

  • To determine the crystal structure of SCIN and identify its active site.
  • To elucidate the specific residues responsible for SCIN's complement inhibitory activity.
  • To explore the therapeutic potential of SCIN in anti-inflammatory treatments.

Main Methods:

  • X-ray crystallography to determine SCIN structure at 1.8 A resolution.
  • Construction and functional characterization of SCIN-homologue chimeric proteins.

Related Experiment Videos

  • Assays to measure inhibition of complement activation pathways (C3a, C5a, C3b, C5b-9 deposition).

    • Main Results:

    • The crystal structure of SCIN was determined, revealing its active site.
    • An 18-residue segment (Leu-31-Gly-48) was identified as critical for SCIN's inhibitory function across all complement pathways.
    • Chimeras lacking these residues failed to inhibit C5a production and showed reduced inhibition of opsonization and membrane attack complex formation.
    • SCIN's stabilization of complement convertases is pivotal for its inhibitory activity.

    Conclusions:

    • SCIN utilizes a specific 18-residue segment for potent inhibition of complement activation.
    • This segment is essential for blocking inflammation (C5a production) and key steps in complement pathways.
    • SCIN's specific and efficient complement inhibition highlights its potential for anti-inflammatory therapies.