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Host Sialic Acids: A Delicacy for the Pathogen with Discerning Taste

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  • Authors: Brandy L. Haines-Menges1, W. Brian Whitaker2, J.B. Lubin3, E. Fidelma Boyd4
  • Editors: Tyrrell Conway5, Paul Cohen6
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Department of Biological Sciences, University of Delaware, Newark, DE 19716, United States; 2: Department of Biological Sciences, University of Delaware, Newark, DE 19716, United States; 3: Department of Biological Sciences, University of Delaware, Newark, DE 19716, United States; 4: Department of Biological Sciences, University of Delaware, Newark, DE 19716, United States; 5: Oklahoma State University, Stillwater, OK; 6: University of Rhode Island, Kingston, RI
  • Source: microbiolspec July 2015 vol. 3 no. 4 doi:10.1128/microbiolspec.MBP-0005-2014
  • Received 07 February 2014 Accepted 16 April 2014 Published 02 July 2015
  • E.F. Boyd, fboyd@udel.edu
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  • Abstract:

    Sialic acids, or the more broad term nonulosonic acids, comprise a family of nine-carbon keto-sugars ubiquitous on mammalian mucous membranes as terminal modifications of mucin glycoproteins. Sialic acids have a limited distribution among bacteria, and the ability to catabolize sialic acids is mainly confined to pathogenic and commensal species. This ability to utilize sialic acid as a carbon source is correlated with bacterial virulence, especially, in the sialic acid rich environment of the oral cavity, respiratory, intestinal, and urogenital tracts. This chapter discusses the distribution of sialic acid catabolizers among the sequenced bacterial genomes and examines the studies that have linked sialic acid catabolism with increased fitness in a number of species using several animal models. This chapter presents the most recent findings in sialobiology with a focus on sialic acid catabolism, which demonstrates an important relationship between the catabolism of sialic acid and bacterial pathogenesis.

  • Citation: Haines-Menges B, Whitaker W, Lubin J, Boyd E. 2015. Host Sialic Acids: A Delicacy for the Pathogen with Discerning Taste. Microbiol Spectrum 3(4):MBP-0005-2014. doi:10.1128/microbiolspec.MBP-0005-2014.

Key Concept Ranking

Sialic Acids
0.5626568
Major Facilitator Superfamily
0.50284094
Polysialic Acid
0.4709764
0.5626568

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/content/journal/microbiolspec/10.1128/microbiolspec.MBP-0005-2014
2015-07-02
2017-11-23

Abstract:

Sialic acids, or the more broad term nonulosonic acids, comprise a family of nine-carbon keto-sugars ubiquitous on mammalian mucous membranes as terminal modifications of mucin glycoproteins. Sialic acids have a limited distribution among bacteria, and the ability to catabolize sialic acids is mainly confined to pathogenic and commensal species. This ability to utilize sialic acid as a carbon source is correlated with bacterial virulence, especially, in the sialic acid rich environment of the oral cavity, respiratory, intestinal, and urogenital tracts. This chapter discusses the distribution of sialic acid catabolizers among the sequenced bacterial genomes and examines the studies that have linked sialic acid catabolism with increased fitness in a number of species using several animal models. This chapter presents the most recent findings in sialobiology with a focus on sialic acid catabolism, which demonstrates an important relationship between the catabolism of sialic acid and bacterial pathogenesis.

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Figures

Image of FIGURE 1
FIGURE 1

Bacterial sialylation of surface components. This diagram depicts the different surface structures in bacteria that are known to be decorated with nonulosonic acids (neuraminic, pseudaminic, or legionaminic). Also indicated are bacterial species demonstrated to have different surfaces sialylated. doi:10.1128/microbiolspec.MBP-0005-2014.f1

Source: microbiolspec July 2015 vol. 3 no. 4 doi:10.1128/microbiolspec.MBP-0005-2014
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Image of FIGURE 2
FIGURE 2

Schematic representation of the catabolism of sialic acid in Bacteria. The first step in catabolism is the uptake into the bacterial cell of free sialic acid molecules across the cell wall and cell membrane. Four type of transport systems have been described for transport across the cell membrane, MFS, SSS, TRAP, and ABC systems. NanH, Neuraminidase; Neu5Ac, -acetylneuraminic acid. The sialic acid catabolic pathway involves several steps beginning with NanA. NanA, -acetylneuraminic acid lyase; ManNAc, -acetylmannosamine; NanK, -acetylmannosamine kinase; ManNAc-6-P, -acetylmannosamine-6-phosphate; NanE, -acetylmannosamine-6-P epimerase; GlcNAc-6-P, -acetylglucosamine-6-phosphate; NagA, -acetylglucosamine-6-phosphate deacteylase; GlcN-6-P, Glucosamine-6-phosphate; NagB, Glucosamine-6-phosphate deaminase; Fru-6-P, Fructose-6-phosphate; LPS, lipopolysaccharide. doi:10.1128/microbiolspec.MBP-0005-2014.f2

Source: microbiolspec July 2015 vol. 3 no. 4 doi:10.1128/microbiolspec.MBP-0005-2014
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Image of FIGURE 3
FIGURE 3

sialic acid metabolism. is an extracellular intestinal pathogen that colonizes the mucus layer of the small intestine and elaborates cholera toxin and sialidase. Sialidase cleaves sialic acid from high order gangliosides to release sialic acid and expose the GM1 ganglioside, the receptor for cholera toxin. Free sialic acid can be transported into the cell via the TRAP transporter SiaPQM contained on the pathogenicity island VPI-2, which also contains the genes for sialic acid catabolism. doi:10.1128/microbiolspec.MBP-0005-2014.f3

Source: microbiolspec July 2015 vol. 3 no. 4 doi:10.1128/microbiolspec.MBP-0005-2014
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Image of FIGURE 4
FIGURE 4

Schematic diagram of the pathogenicity island VPI-2 in choleragenic isolates. ORFs of interest are depicted as arrows indicting the direction of transcription. The entire sialic acid catabolism cluster encompasses 12 kb on the 57 kb VPI-2 region. doi:10.1128/microbiolspec.MBP-0005-2014.f4

Source: microbiolspec July 2015 vol. 3 no. 4 doi:10.1128/microbiolspec.MBP-0005-2014
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Tables

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TABLE 1

Bacterial species in which sialic acid catabolism was experimentally examined

Source: microbiolspec July 2015 vol. 3 no. 4 doi:10.1128/microbiolspec.MBP-0005-2014

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