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Infection and Immunity, September 2009, p. 3807-3816, Vol. 77, No. 9
0019-9567/09/$08.00+0     doi:10.1128/IAI.00279-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Sialic Acid Catabolism Confers a Competitive Advantage to Pathogenic Vibrio cholerae in the Mouse Intestine{triangledown}

Salvador Almagro-Moreno1,2 and E. Fidelma Boyd1*

Department of Biological Sciences, University of Delaware, Newark, Delaware 19716,1 Department of Microbiology, National University of Ireland, Cork, Ireland2

Received 10 March 2009/ Returned for modification 12 April 2009/ Accepted 7 June 2009

Sialic acids comprise a family of nine-carbon ketosugars that are ubiquitous on mammalian mucous membranes. However, sialic acids have a limited distribution among Bacteria and are confined mainly to pathogenic and commensal species. Vibrio pathogenicity island 2 (VPI-2), a 57-kb region found exclusively among pathogenic strains of Vibrio cholerae, contains a cluster of genes (nan-nag) putatively involved in the scavenging (nanH), transport (dctPQM), and catabolism (nanA, nanE, nanK, and nagA) of sialic acid. The capacity to utilize sialic acid as a carbon and energy source might confer an advantage to V. cholerae in the mucus-rich environment of the gut, where sialic acid availability is extensive. In this study, we show that V. cholerae can utilize sialic acid as a sole carbon source. We demonstrate that the genes involved in the utilization of sialic acid are located within the nan-nag region of VPI-2 by complementation of Escherichia coli mutants and gene knockouts in V. cholerae N16961. We show that nanH, dctP, nanA, and nanK are highly expressed in V. cholerae grown on sialic acid. By using the infant mouse model of infection, we show that V. cholerae {Delta}nanA strain SAM1776 is defective in early intestinal colonization stages. In addition, SAM1776 shows a decrease in the competitive index in colonization-competition assays comparing the mutant strain with both O1 El Tor and classical strains. Our data indicate an important relationship between the catabolism of sialic acid and bacterial pathogenesis, stressing the relevance of the utilization of the resources found in the host's environment.

* Corresponding author. Mailing address: Department of Biological Sciences, 328 Wolf Hall, University of Delaware, Newark, DE 19716. Phone: (302) 831-1088. Fax: (302) 831-2281. E-mail: fboyd{at}udel.edu

{triangledown} Published ahead of print on 29 June 2009.

Editor: A. Camilli

Infection and Immunity, September 2009, p. 3807-3816, Vol. 77, No. 9
0019-9567/09/$08.00+0     doi:10.1128/IAI.00279-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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