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Infection and Immunity, July 2006, p. 4094-4103, Vol. 74, No. 7
0019-9567/06/$08.00+0     doi:10.1128/IAI.00433-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

{alpha}-2,3-Sialyltransferase Enhances Neisseria gonorrhoeae Survival during Experimental Murine Genital Tract Infection

Hong Wu and Ann E. Jerse*

Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814-4799

Received 16 March 2006/ Returned for modification 13 April 2006/ Accepted 3 May 2006

The addition of host-derived sialic acid to Neisseria gonorrhoeae lipooligosaccharide is hypothesized to be an important mechanism by which gonococci evade host innate defenses. This hypothesis is based primarily on in vitro assays of complement-mediated and phagocytic killing. Here we report that a nonpolar {alpha}-2,3-sialyltransferase (lst) mutant of N. gonorrhoeae was significantly attenuated in its capacity to colonize the lower genital tract of 17-ß estradiol-treated female BALB/c mice during competitive infection with the wild-type strain. Genetic complementation of the lst mutation restored recovery of the mutant to wild-type levels. Studies with B10.D2-HCoH2dH2-T18c/OSN (C5-deficient) mice showed that attenuation of the lst mutant was not due to increased sensitivity to complement-mediated bacteriolysis, a result that is consistent with recently reported host restrictions in the complement cascade. However, Lst-deficient gonococci were killed more rapidly than sialylated wild-type gonococci following intraperitoneal injection into normal mice, which is consistent with sialylation conferring protection against killing by polymorphonuclear leukocytes (PMNs). As reported for human PMNs, sialylated gonococci were more resistant to killing by murine PMNs, and sialylation led to reduced association with and induction of a weaker respiratory burst in PMNs from estradiol-treated mice. In summary, these studies suggest sialylation confers a survival advantage to N. gonorrhoeae in mice by increasing resistance to PMN killing. This report is the first direct demonstration that {alpha}-2,3-sialyltransferase contributes to N. gonorrhoeae pathogenesis in an in vivo model. This study also validates the use of experimental murine infection to study certain aspects of gonococcal pathogenesis.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Rd., Bethesda, MD 20814-4799. Phone: (301) 295-9629. Fax: (301) 295-3773. E-mail: ajerse{at}usuhs.mil.

Editor: V. J. DiRita

Infection and Immunity, July 2006, p. 4094-4103, Vol. 74, No. 7
0019-9567/06/$08.00+0     doi:10.1128/IAI.00433-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Wu, H., Soler-Garcia, A. A., Jerse, A. E. (2009). A Strain-Specific Catalase Mutation and Mutation of the Metal-Binding Transporter Gene mntC Attenuate Neisseria gonorrhoeae In Vivo but Not by Increasing Susceptibility to Oxidative Killing by Phagocytes. Infect. Immun. 77: 1091-1102 [Abstract] [Full Text]  
  • Smith, H., Tang, C. M., Exley, R. M. (2007). Effect of Host Lactate on Gonococci and Meningococci: New Concepts on the Role of Metabolites in Pathogenicity. Infect. Immun. 75: 4190-4198 [Full Text]  
  • Soler-Garcia, A. A., Jerse, A. E. (2007). Neisseria gonorrhoeae Catalase Is Not Required for Experimental Genital Tract Infection despite the Induction of a Localized Neutrophil Response. Infect. Immun. 75: 2225-2233 [Abstract] [Full Text]  
  • Exley, R. M., Wu, H., Shaw, J., Schneider, M. C., Smith, H., Jerse, A. E., Tang, C. M. (2007). Lactate Acquisition Promotes Successful Colonization of the Murine Genital Tract by Neisseria gonorrhoeae. Infect. Immun. 75: 1318-1324 [Abstract] [Full Text]  


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