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Originally published In Press as doi:10.1074/jbc.M006883200 on April 16, 2001

J. Biol. Chem., Vol. 276, Issue 26, 24331-24340, June 29, 2001
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Pathogenic Neisseria Trigger Expression of Their Carcinoembryonic Antigen-related Cellular Adhesion Molecule 1 (CEACAM1; Previously CD66a) Receptor on Primary Endothelial Cells by Activating the Immediate Early Response Transcription Factor, Nuclear Factor-kappa B*

Petra MuenznerDagger §, Michael Naumann§, Thomas F. MeyerDagger §, and Scott D. Gray-Owen||**

From the Dagger  Max-Planck-Institut für Biologie, Abteilung Infektionsbiologie, Spemannstrasse 34, 72076 Tübingen, the § Max-Planck-Institut für Infektionsbiologie, Abteilung Molekulare Biologie, Schumannstrasse 21/22, Berlin (Mitte) D-10117, Germany, and the || Department of Medical Genetics and Microbiology, University of Toronto, Toronto M5S 1A8, Canada.

Neisseria gonorrhoeae express opacity-associated (Opa) protein adhesins that mediate binding to various members of the carcinoembryonic antigen-related cellular adhesion molecule (CEACAM; previously CD66) receptor family. Although human umbilical vein endothelial cells express little CEACAM receptor in vitro, we found neisserial infection to induce expression of CEACAM1, CEACAM1-3L, and CECAM1-4L splice variants. This mediates an increased Opa52-dependent binding of gonococci by these cells. The induced receptor expression did not require bacterial Opa expression, but it was more rapid with adherent bacteria. Because the time course of induction was similar to that seen for induced proinflammatory cytokines, we tested whether CEACAM1 expression could be controlled by a similar mechanism. Gonococcal infection activated a nuclear factor-kappa B (NF-kappa B) heterodimer consisting of p50 and p65, and inhibitors that prevent the nuclear translocation of activated NF-kappa B complex inhibited CEACAM1 transcript expression. Each of these effects could be mimicked by using culture filtrates or purified lipopolysaccharide instead of intact bacteria. Together, our results support a model whereby the outer membrane "blebs" that are actively released by gonococci trigger a Toll-like receptor-4-dependent activation of NF-kappa B, which up-regulates the expression of CEACAM1 to allow Opa52-mediated neisserial binding. The regulation of CEACAM1 expression by NF-kappa B also implies a broader role for this receptor in the general inflammatory response to infection.

* This study was supported in part by Deutsche Forschungsgemeinschaft Grants Me705/5-1 and Na292/5-2 and by the Fonds der Chemischen Industrie.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed in Berlin. Tel.: 49-030-2846-0402; Fax: 49-030-2846-0401; E-mail: meyer@mpiib-berlin.mpg.de.

** Supported by Medical Research Council of Canada Grant MT-15499.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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