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Originally published In Press as doi:10.1074/jbc.M010609200 on February 5, 2001

J. Biol. Chem., Vol. 276, Issue 20, 17413-17419, May 18, 2001
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The CGM1a (CEACAM3/CD66d)-mediated Phagocytic Pathway of Neisseria gonorrhoeae Expressing Opacity Proteins Is Also the Pathway to Cell Death*

Tie ChenDagger §, Silvia Bolland, Ines Chen||, James Parker||, Milica PantelicDagger , Fritz Grunert**, and Wolfgang Zimmermann**

From the Dagger  Department of Microbiology, Immunology and Medicine, Walther Oncology Center, Indiana University School of Medicine, Indianapolis, Indiana 46202, the || Laboratory of Bacterial Pathogenesis and Immunology, the  Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York, New York 10021, and the ** Institute of Molecular Medicine and Cell Research, University of Freiburg, D-79104 Freiburg, Germany

Phagocytosis of Opa+ Neisseria gonorrhoeae (gonococcus, GC) by neutrophils is in part dependent on the interaction of Opa proteins with CGM1a (CEACAM3/CD66d) antigens, a neutrophil-specific receptor. However, the signaling pathways leading to phagocytosis have not been characterized. Here we show that interaction of OpaI bacteria with neutrophils or CGM1a-transfected DT40 cells induces calcium flux, which correlates with phagocytosis of bacteria. We identified an immunoreceptor tyrosine-based activation motif (ITAM) in CGM1a, and showed that the ability of CGM1a to transduce signals and mediate phagocytosis was abolished by mutation of the ITAM tyrosines. We also demonstrated that CGM1a-ITAM-mediated bacterial phagocytosis is dependent on Syk and phospholipase C activity in DT40 cells. Unexpectedly, the activation of the CGM1a-ITAM phagocytic pathway by Opa+ GC results in induction of cell death.

* This work was supported by Public Health Service Grants AI 47736 (to T. C.) and AI 26558 (to E. G.) and a grant from the Deutsche Forschungsgemeinschaft (to W. Z.).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: Dept. of Microbiology, Immunology, and Medicine, Indiana University School of Medicine, MS 252, 635 Barnhill Dr., Indianapolis, IN 46202-5120. Tel.: 317-274-0519; Fax: 317-274-4090; E-mail: tiechen@iupui.edu.

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