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Infection and Immunity, March 2009, p. 1091-1102, Vol. 77, No. 3
0019-9567/09/$08.00+0     doi:10.1128/IAI.00825-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

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{triangledown}

Hong Wu, Ángel A. Soler-García,{dagger} and Ann E. Jerse*

Department of Microbiology and Immunology, F. Edward Hebert School of Medicine, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20814

Received 3 July 2008/ Returned for modification 29 September 2008/ Accepted 19 December 2008

The hallmark of gonorrhea is an intense inflammatory response that is characterized by polymorphonuclear leukocytes (PMNs) with intracellular gonococci. A redundancy of defenses may protect Neisseria gonorrhoeae from phagocyte-derived reactive oxygen species. Here we showed that a gonococcal catalase (kat) mutant in strain MS11 was more sensitive to H2O2 than mutants in cytochrome c peroxidase (ccp), methionine sulfoxide reductase (msrA), or the metal-binding protein (mntC) of the MntABC transporter. kat ccp and kat ccp mntC mutants were significantly more sensitive to H2O2 than mutants in any single factor. None of the mutants showed increased susceptibility to murine PMNs. Recovery of the mntC and kat ccp mntC mutants from the lower genital tract of BALB/c mice, but not the kat or kat ccp mutants, was significantly reduced relative to wild-type bacteria. Interestingly, unlike the MS11 kat mutant, a kat mutant of strain FA1090 was attenuated during competitive infection with wild-type FA1090 bacteria. The FA1090 kat mutant and MS11 mntC mutant were also attenuated in mice that are unable to generate a phagocytic respiratory burst. We conclude that inactivation of three well-characterized antioxidant genes (kat, ccp, and mntC) does not increase gonococcal susceptibility to the phagocytic respiratory burst during infection and that gonococcal catalase and the MntC protein confer an unidentified advantage in vivo. In the case of catalase, this advantage is strain specific. Finally, we also showed that an msrA mutant of strain MS11 demonstrated delayed attenuation in BALB/c but not C57BL/6 mice. Therefore, MsrA/B also appears to play a role in infection that is dependent on host genetic background.

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

{triangledown} Published ahead of print on 29 December 2008.

Editor: J. N. Weiser

{dagger} Present address: Center for Genetic Medicine Research, Division of Nephrology, Children's Research Institute, Children's National Medical Center, 111 Michigan Ave., NW, Washington, DC 20010.

Infection and Immunity, March 2009, p. 1091-1102, Vol. 77, No. 3
0019-9567/09/$08.00+0     doi:10.1128/IAI.00825-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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