The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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Published online 3 July 2006 doi:10.1084/jem.20060565
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 7, 1671-1677
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BRIEF DEFINITIVE REPORT

 ESAM supports neutrophil extravasation, activation of Rho, and VEGF-induced vascular permeability

Frank Wegmann1, Björn Petri1, Alexander Georg Khandoga2, Christian Moser2, Andrej Khandoga2, Stefan Volkery1, Hang Li1, Ines Nasdala1, Oliver Brandau3, Reinhard Fässler3, Stefan Butz1, Fritz Krombach2, and Dietmar Vestweber1

1 Max-Planck-Institute for Molecular Biomedicine and Institute of Cell Biology, University of Münster, D-48149 Münster, Germany
2 Institute for Surgical Research, University of Munich, D-81377 Munich, Germany
3 Max-Planck-Institute for Biochemistry, D-82152 Martinsried, Germany

CORRESPONDENCE Dietmar Vestweber: vestweb{at}uni-muenster.de OR Stefan Butz: butzs{at}uni-muenster.de

Endothelial cell–selective adhesion molecule (ESAM) is specifically expressed at endothelial tight junctions and on platelets. To test whether ESAM is involved in leukocyte extravasation, we have generated mice carrying a disrupted ESAM gene and analyzed them in three different inflammation models. We found that recruitment of lymphocytes into inflamed skin was unaffected by the gene disruption. However, the migration of neutrophils into chemically inflamed peritoneum was inhibited by 70% at 2 h after stimulation, recovering at later time points. Analyzing neutrophil extravasation directly by intravital microscopy in the cremaster muscle revealed that leukocyte extravasation was reduced (50%) in ESAM–/– mice without affecting leukocyte rolling and adhesion. Depletion of >98% of circulating platelets did not abolish the ESAM deficiency–related inhibitory effect on neutrophil extravasation, indicating that it is only ESAM at endothelial tight junctions that is relevant for the extravasation process. Knocking down ESAM expression in endothelial cells resulted in reduced levels of activated Rho, a GTPase implicated in the destabilization of tight junctions. Indeed, vascular permeability stimulated by vascular endothelial growth factor was reduced in ESAM–/– mice. Collectively, ESAM at endothelial tight junctions participates in the migration of neutrophils through the vessel wall, possibly by influencing endothelial cell contacts.

F. Wegmann and B. Petri contributed equally to this work.


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