The Journal of Experimental Medicine
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Published 1 March 2004. doi:10.1084/jem.20031636
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 199, Number 5, 687-695
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Chemotaxis Inhibitory Protein of Staphylococcus aureus, a Bacterial Antiinflammatory Agent

Carla J.C. de Haas1, Karin Ellen Veldkamp1, Andreas Peschel1,2, Floor Weerkamp1, Willem J.B. Van Wamel1, Erik C.J.M. Heezius1, Miriam J.J.G. Poppelier1, Kok P.M. Van Kessel1, and Jos A.G. van Strijp1

1 Eijkman-Winkler Institute, University Medical Center Utrecht, 3584 CX Utrecht, Netherlands
2 Cellular and Molecular Microbiology, Medical Microbiology and Hygiene Department, University of Tübingen, 72076 Tübingen, Germany

Address correspondence to Jos A.G. van Strijp, Eijkman-Winkler Institute, Room G04-614, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, Netherlands. Phone: 31-30-2506528; Fax: 31-30-2541770; email: j.vanstrijp{at}azu.nl

Leukocyte migration is a key event both in host defense against invading pathogens as well as in inflammation. Bacteria generate chemoattractants primarily by excretion (formylated peptides), complement activation (C5a), and subsequently through activation of leukocytes (e.g., leukotriene B4, platelet-activating factor, and interleukin 8). Here we describe a new protein secreted by Staphylococcus aureus that specifically impairs the response of neutrophils and monocytes to formylated peptides and C5a. This chemotaxis inhibitory protein of S. aureus (CHIPS) is a 14.1-kD protein encoded on a bacteriophage and is found in >60% of clinical isolates. CHIPS reduces the neutrophil recruitment toward C5a in a mouse peritonitis model, even though its activity is much more potent on human than on mouse cells. These findings suggest a new immune escape mechanism of S. aureus and put forward CHIPS as a potential new antiinflammatory therapeutic compound.

Key Words: Staphylococcus aureus • phagocytes • chemotaxis • C5a • formylated peptides

C.J.C. de Haas and K.E. Veldkamp contributed equally to this work.

Abbreviations used in this paper: BODIPY, boron dipyrromethane; CHIPS, chemotaxis inhibitory protein of Staphylococcus aureus; Eap, extracellular adherence protein; GPCR, G protein–coupled receptor; HSA, human serum albumin; MIP-1{alpha}, macrophage inflammatory protein 1{alpha}; PAF, platelet-activating factor.


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