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Originally published online as doi:10.1189/jlb.0405184 on February 3, 2006

Published online before print February 3, 2006
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(Journal of Leukocyte Biology. 2006;79:731-738.)
© 2006 by Society for Leukocyte Biology

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§,1 and Tie Chen*,2

* 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
§ Molecular Epidemiology, Enteric Diseases Research Program, U.S. Naval Medical Research Unit-3, Cairo, Egypt

1Corresponding author: Enteric Diseases Research Program, U.S. Naval Medical Research Unit-3, PSC452, Box 154, FPO AE 09835, Cairo, Egypt. E-mail: KlenaJ{at}namru3.med.navy.mil

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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