Journal of Leukocyte Biology
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A more recent version of this article appeared on April 1, 2006

Published online before print February 3, 2006
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0405184


Received for publication April 10, 2005.
Revised September 20, 2005.
Accepted for publication October 19, 2005.


Article

DC-SIGN (CD209) recognition of Neisseria gonorrhoeae is circumvented by lipooligosaccharide variation

Pei Zhang *, Olivier Schwartz {dagger}, Milica Pantelic {ddagger}, Geling Li {ddagger}, Quita Knazze {ddagger}, Cinzia Nobile {dagger}, Milan Radovich {ddagger}, Johnny He {ddagger}, Soon-Cheol Hong {ddagger}, John Klena {sect}@, and Tie Chen *@

*Department of Biomedical Sciences, College of Medicine, University of Illinois at Chicago; {dagger}Virus and Immunity Group in the Department of Virology, Institut Pasteur, France; {ddagger}Department of Microbiology and Immunology, Division of Infectious Diseases, Walther Oncology Center, Indiana University School of Medicine, Indianapolis; and {sect}Molecular Epidemiology, Enteric Diseases Research Program, U.S. Naval Medical Research Unit-3, Cairo, Egypt

@ To whom correspondence should be addressed. E-mail: KlenaJ{at}namru3.med.navy.mil.


   Abstract

Neisseria gonorrhoeae (GC) or Escherichia coli HB101 (hereafter referred to as E. coli) expressing opacity (Opa) proteins adhere to human host cells and stimulate phagocytosis as a result of the interaction of certain Opa proteins to carcinoembryonic antigen-related cellular adhesion molecule 1 (CEACAM1; CD66a) receptors. Our experiments show that the Opa-CEACAM1 interaction does not play a significant role in adherence between these bacteria and dendritic cells (DCs). Instead, phagocytosis of GC and E. coli by DCs is mediated by the DC-specific intercellular adhesion molecule-grabbing nonintegrin, (SIGN; CD209) receptor. DC-SIGN recognition and subsequent phagocytosis of GC are limited, however, to a lipooligosaccharide (LOS) mutant (lgtB) of GC. This conclusion is supported by experiments demonstrating that HeLa cells expressing human DC-SIGN (HeLa-DC-SIGN) bind exclusively to and engulf an lgtB mutant of GC, and this interaction is blocked specifically by an anti-DC-SIGN antibody. The experiments suggest that LOS variation may have evolved as a mechanism for GC to avoid phagocytosis by DCs.

Key Words: Escherichia coli • dendritic cells • CEACAM1 (CD66a)




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