The Journal of Experimental Medicine
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Published online 3 April 2006. doi:10.1084/jem.20051681
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© The Rockefeller University Press, 0022-1007
The Journal of Experimental Medicine

ARTICLE

Suppression of experimental autoimmune encephalomyelitis by extracellular adherence protein of Staphylococcus aureus

Changping Xie2, Pilar Alcaide4, Brian V. Geisbrecht3, Darius Schneider2, Mathias Herrmann5, Klaus T. Preissner6, Francis W. Luscinskas4, and Triantafyllos Chavakis1

1 Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892
2 Department of Internal Medicine I, University Heidelberg, D-69120 Heidelberg, Germany
3 Division of Cell Biology and Biophysics, School of Biological Sciences, University of Missouri-Kansas City, Kansas City, MO 64110
4 Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115
5 Institute of Medical Microbiology and Hygiene, University of Saarland Hospital, D-66421 Homburg/Saar, Germany
6 Institute for Biochemistry, Medical School, Justus-Liebig-University, D-35392 Giessen, Germany

CORRESPONDENCE Triantafyllos Chavakis: chavakist{at}mail.nih.gov

Multiple sclerosis (MS) is a devastating inflammatory disorder of the central nervous system (CNS). A major hallmark of MS is the infiltration of T cells reactive against myelin components. T cell infiltration is mediated by the interaction of integrins of the ß1 and ß2 family expressed by lymphocytes with their endothelial counter-receptors, vascular cell adhesion molecule 1 and intercellular adhesion molecule (ICAM)-1, respectively. We have reported previously that extracellular adherence protein (Eap) of Staphylococcus aureus exerts antiinflammatory activities by interacting with ICAM-1 and blocking ß2-integrin–dependent neutrophil recruitment. Here, we report that Eap inhibits experimental autoimmune encephalomyelitis (EAE) in mice. In vitro, Eap reduced adhesion of peripheral blood T cells to immobilized ICAM-1 as well as their adhesion and transmigration of TNF-activated human endothelium under static and shear flow conditions. These inhibitory effects were corroborated in two mouse models of inflammation. In a delayed-type hypersensitivity model, both T cell infiltration and the corresponding tissue edema were significantly reduced by Eap. In addition, Eap administration prevented the development of EAE and markedly decreased infiltration of inflammatory cells into the CNS. Strikingly, intervention with Eap after the onset of EAE suppressed the disease. Collectively, our findings indicate that Eap represents an attractive treatment for autoimmune neuroinflammatory disorders such as MS.

Abbreviations used: BBB, blood–brain barrier; CNS, central nervous system; DTH, delayed-type hypersensitivity; EAE, experimental autoimmune encephalomyelitis; Eap, extracellular adherence protein; HUVEC, human umbilical vein endothelial cell; ICAM, intercellular adhesion molecule; MOG, myelin oligodendrocyte glycoprotein; MS, multiple sclerosis; PBT, peripheral blood T; VCAM, vascular cell adhesion molecule.


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