title: N-acetylneuraminic acid transport by Streptococcus oralis strain AR3.
abstract: Streptococcus oralis has emerged as one of the most important organisms of the viridans streptococcus group in terms of infections and is recognised as an agent of infective endocarditis and, in immunocompromised patients, septicaemia. The mechanisms by which this organism proliferates in vivo are unknown. However, host-derived sialic acids -- including N-acetylneuraminic acid (NeuNAc) which is present in serum and cell-associated glycoproteins -- are a potential source of fermentable carbohydrate for bacterial proliferation, especially for sialidase-producing bacteria, including S. oralis. To further elucidate the role of NeuNAc in supporting growth, this study determined the ability of S. oralis strain AR3 (isolated from a patient with infective endocarditis) to transport NeuNAc and characterised the transport system. The transport of [14C]-labelled NeuNAc into S. oralis was monitored and this transport system was induced by growth of the bacteria in the presence of the N-acetylated sugars NeuNAc, N-acetylglucosamine and N-acetylmannosamine. The transport system followed typical Michaelis-Menten kinetics, with a Km of 21.0 microM and a Vmax of 2.65 nmoles of NeuNAc transported/min/mg of dry cell mass. NeuNAc transport was inhibited by the presence of exogenous N-glycolylneuraminic acid, a related sialic acid. Chlorhexidine, NaF and 2,4-dinitrophenol were potent inhibitors of the transport system, suggesting that the uptake of NeuNAc occurs via a proton motive force-dependent permease system. This is the first report of the mechanism by which NeuNAc transport occurs in pathogenic streptococci. This transport process may have relevance to the acquisition of a source of fermentable carbohydrate and thus bacterial proliferation in vivo.
authors.forename: H L
authors.initials: HL
authors.lastname: Byers
authors.forename: K A
authors.initials: KA
authors.lastname: Homer
authors.forename: E
authors.initials: E
authors.lastname: Tarelli
authors.forename: D
authors.initials: D
authors.lastname: Beighton
mesh_terms: D019297:2,4-Dinitrophenol / Q000494:pharmacology; D000117:Acetylglucosamine / Q000378:metabolism; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D001149:Arsenates / Q000494:pharmacology; D001692:Biological Transport; D002710:Chlorhexidine / Q000494:pharmacology; D004697:Endocarditis, Bacterial / Q000382:microbiology*; D006595:Hexosamines / Q000378:metabolism; D006801:Humans; D007700:Kinetics; D009005:Monosaccharides / Q000378:metabolism; D019158:N-Acetylneuraminic Acid / Q000378:metabolism*; D018892:Proton-Motive Force / Q000187:drug effects; D015203:Reproducibility of Results; D019810:Sodium Azide / Q000494:pharmacology; D012969:Sodium Fluoride / Q000494:pharmacology; D013290:Streptococcal Infections / Q000382:microbiology*; D019533:Streptococcus oralis / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism*; D014475:Uncoupling Agents / Q000494:pharmacology
chemical_list: D000900:Anti-Bacterial Agents; D001149:Arsenates; D006595:Hexosamines; D009005:Monosaccharides; D014475:Uncoupling Agents; C009277:sodium arsenate; D012969:Sodium Fluoride; D019810:Sodium Azide; D019158:N-Acetylneuraminic Acid; D019297:2,4-Dinitrophenol; D002710:Chlorhexidine; D000117:Acetylglucosamine; C002022:N-acetylmannosamine