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Infect. Immun. doi:10.1128/IAI.01530-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Lactate acquisition promotes the successful colonisation of the murine genital tract by Neisseria gonorrhoeae

The Centre for Molecular Microbiology and Infection, Department of Infectious Diseases, Flowers Building, Imperial College London, Armstrong Road, London, SW7 2AZ, U.K.; Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University, Bethesda, Maryland 20814, USA; Division of Genomic Medicine, F-floor, University of Sheffield Medical School, Beech Hill Road, Sheffield, S10 2RX, U.K.; The Medical School, University of Birmingham, Edgbaston, Birmingham, B15 2TT, U.K.
The Centre for Molecular Microbiology and Infection, Department of Infectious Diseases, Flowers Building, Imperial College London, Armstrong Road, London, SW7 2AZ, U.K.; Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University, Bethesda, Maryland 20814, USA; Division of Genomic Medicine, F-floor, University of Sheffield Medical School, Beech Hill Road, Sheffield, S10 2RX, U.K.; The Medical School, University of Birmingham, Edgbaston, Birmingham, B15 2TT, U.K.

^* To whom correspondence should be addressed. Email: ajerse{at}usuhs.mil, c.tang{at}imperial.ac.uk.

	Abstract

Previous studies on Neisseria gonorrhoeae have demonstrated that metabolism of lactate in the presence of glucose increases the growth rate of the bacterium and enhances its resistance against complement-mediated killing. Although these findings in vitro suggest that the acquisition of lactate promotes gonococcal colonisation, the significance of this carbon source to the survival of the gonococcus in vivo remains unknown. To investigate the importance of lactate utilisation during Neisseria gonorrhoeae genital tract infection, we identified the gene, lctP, which encodes the gonococcal lactate permease. A mutant that lacks a functional copy of lctP was unable to take up exogenous lactate and did not grow in defined medium with lactate as the sole carbon source in contrast to the wild-type and complemented strains; the mutant strain exhibited no growth defect in defined medium containing glucose. In defined medium containing physiological concentrations of lactate and glucose, the lctP mutant demonstrated reduced early growth and increased sensitivity to complement-mediated killing compared with the wild-type strain; the enhanced susceptibility to complement was associated with a reduction in lipopolysaccharide sialylation of the lctP mutant. The importance of lactate utilisation during colonisation was evaluated in the murine model of lower genital tract infection. The lctP mutant was significantly attenuated in its ability to colonise and survive in the genital tract while the complemented mutant exhibited no defect for colonisation. Lactate is a micronutrient in the genital tract that contributes to the survival of the gonococcus.

This article has been cited by other articles:

• 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]