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Infection and Immunity, July 2005, p. 4171-4179, Vol. 73, No. 7
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.7.4171-4179.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Neisseria gonorrhoeae Kills Carcinoembryonic Antigen-Related Cellular Adhesion Molecule 1 (CD66a)-Expressing Human B Cells and Inhibits Antibody Production

Milica Pantelic,1 Young-June Kim,1 Silvia Bolland,2 Ines Chen,3 John Shively,4 and Tie Chen1*

Department of Microbiology and Immunology, Division of Infectious Diseases, Walther Oncology Center, Indiana University School of Medicine, Indianapolis, Indiana,1 Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, NIH, 12441 Parklawn Drive, Twinbrook II, Room 217, Rockville, Maryland,2 Public Health Research Institute, 225 Warren Street, Newark, New Jersey,3 Division of Immunology, Beckman Research Institute of the City of Hope, Duarte, California4

Received 13 September 2004/ Returned for modification 15 November 2004/ Accepted 19 January 2005

Neisseria gonorrhoeae cells (gonococci [GC]), the etiological agents for gonorrhea, can cause repeated infections. During and after gonococcal infection, local and systemic antigonococcal antibody levels are low. These clinical data indicate the possibility that GC may suppress immune responses during infection. Carcinoembryonic antigen-related cellular adhesion molecule 1 (CEACAM1 or CD66a), a receptor for GC opacity (Opa) proteins, was shown to mediate inhibitory signals. In the present study, human B cells were activated by interleukin-2 to express CEACAM1 and then stimulated to secrete antibodies and simultaneously coincubated with Opa– and OpaI GC of strain MS11. Our results show that this OpaI GC has the ability to inhibit antibody production. The interaction of GC and CEACAM1 with human peripheral B cells also results in induction of cell death. The same findings were observed in DT40 B cells. This CEACAM1-promoted cell death pathway does not involve the inhibitory signals or the tyrosine phosphatases SHP-1 and SHP-2 but depends on Bruton's tyrosine kinase in DT40 cells. Our results suggest that Neisseria gonorrhoeae possesses the ability to suppress antibody production by killing CEACAM1-expressing B cells.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Division of Infectious Diseases, Walther Oncology Center, Indiana University School of Medicine, MS415E, 635 Barnhill Dr., Indianapolis, IN 46202-5120. Phone: (317) 274-0519. Fax: (317) 274-4090. E-mail: tiechen{at}iupui.edu.

Editor: D. L. Burns

Infection and Immunity, July 2005, p. 4171-4179, Vol. 73, No. 7
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.7.4171-4179.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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