The Journal of Experimental Medicine
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Published online
doi:10.1084/jem.20070818
The Journal of Experimental Medicine, Vol. 204, No. 10, 2461-2471
The Rockefeller University Press, 0022-1007 $30.00
© Jongerius et al.
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ARTICLE

 Staphylococcal complement evasion by various convertase-blocking molecules

Ilse Jongerius1, Jörg Köhl2, Manoj K. Pandey2, Maartje Ruyken1, Kok P.M. van Kessel1, Jos A.G. van Strijp1, and Suzan H.M. Rooijakkers1

1 Medical Microbiology, University Medical Center Utrecht, 3584 CX Utrecht, Netherlands
2 Division of Molecular Immunology, Cincinnati Children's Hospital Medical Center and University of Cincinnati College of Medicine, Cincinnati, OH 45229

CORRESPONDENCE Ilse Jongerius: i.jongerius{at}umcutrecht.nl

To combat the human immune response, bacteria should be able to divert the effectiveness of the complement system. We identify four potent complement inhibitors in Staphylococcus aureus that are part of a new immune evasion cluster. Two are homologues of the C3 convertase modulator staphylococcal complement inhibitor (SCIN) and function in a similar way as SCIN. Extracellular fibrinogen-binding protein (Efb) and its homologue extracellular complement-binding protein (Ecb) are identified as potent complement evasion molecules, and their inhibitory mechanism was pinpointed to blocking C3b-containing convertases: the alternative pathway C3 convertase C3bBb and the C5 convertases C4b2aC3b and C3b2Bb. The potency of Efb and Ecb to block C5 convertase activity was demonstrated by their ability to block C5a generation and C5a-mediated neutrophil activation in vitro. Further, Ecb blocks C5a-dependent neutrophil recruitment into the peritoneal cavity in a mouse model of immune complex peritonitis. The strong antiinflammatory properties of these novel S. aureus–derived convertase inhibitors make these compounds interesting drug candidates for complement-mediated diseases.

Abbreviations used: AP, CP, and LP, alternative, classical, and lectin pathway, respectively; CHIPS, chemotaxis inhibitory protein of S. aureus; Ecb, extracellular complement-binding protein; Efb, extracellular fibrinogen-binding protein; Efb-C, C3-binding domain of Efb; EK, enterokinase; fB, fD, and fH, factor B, D, and H, respectively; FLIPr, FPR-like 1 inhibitory protein; FPR, formylated peptide receptor; His, histidine; IC, immune complex; IEC, immune evasion cluster; MAC, membrane attack complex; ORF, open reading frame; PO, peroxidase; SCIN, staphylococcal complement inhibitor; SSL, staphylococcal superantigen like.


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