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    Role of sapA and yfgA in Susceptibility to Antibody-Mediated Complement-Dependent Killing and Virulence of Salmonella enterica Serovar Typhimurium

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    Author
    Ondari, EM; Heath, JN; Klemm, EJ; Langridge, G; Barquist, L; Goulding, DA; Clare, S; Dougan, G; Kingsley, RA; MacLennan, CA
    Date
    2017-09-01
    Source Title
    Infection and Immunity
    Publisher
    AMER SOC MICROBIOLOGY
    University of Melbourne Author/s
    Dougan, Gordon
    Affiliation
    Microbiology and Immunology
    Metadata
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    Document Type
    Journal Article
    Citations
    Ondari, E. M., Heath, J. N., Klemm, E. J., Langridge, G., Barquist, L., Goulding, D. A., Clare, S., Dougan, G., Kingsley, R. A. & MacLennan, C. A. (2017). Role of sapA and yfgA in Susceptibility to Antibody-Mediated Complement-Dependent Killing and Virulence of Salmonella enterica Serovar Typhimurium. INFECTION AND IMMUNITY, 85 (9), https://doi.org/10.1128/IAI.00419-17.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/259650
    DOI
    10.1128/IAI.00419-17
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5563563
    Abstract
    The ST313 pathovar of Salmonella enterica serovar Typhimurium contributes to a high burden of invasive disease among African infants and HIV-infected adults. It is characterized by genome degradation (loss of coding capacity) and has increased resistance to antibody-dependent complement-mediated killing compared with enterocolitis-causing strains of S Typhimurium. Vaccination is an attractive disease-prevention strategy, and leading candidates focus on the induction of bactericidal antibodies. Antibody-resistant strains arising through further gene deletion could compromise such a strategy. Exposing a saturating transposon insertion mutant library of S Typhimurium to immune serum identified a repertoire of S Typhimurium genes that, when interrupted, result in increased resistance to serum killing. These genes included several involved in bacterial envelope biogenesis, protein translocation, and metabolism. We generated defined mutant derivatives using S Typhimurium SL1344 as the host. Based on their initial levels of enhanced resistance to killing, yfgA and sapA mutants were selected for further characterization. The S Typhimurium yfgA mutant lost the characteristic Salmonella rod-shaped appearance, exhibited increased sensitivity to osmotic and detergent stress, lacked very long lipopolysaccharide, was unable to invade enterocytes, and demonstrated decreased ability to infect mice. In contrast, the S Typhimurium sapA mutants had similar sensitivity to osmotic and detergent stress and lipopolysaccharide profile and an increased ability to infect enterocytes compared with the wild type, but it had no increased ability to cause in vivo infection. These findings indicate that increased resistance to antibody-dependent complement-mediated killing secondary to genetic deletion is not necessarily accompanied by increased virulence and suggest the presence of different mechanisms of antibody resistance.

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