TO THE EDITOR—We thank Dupieux et al for their thoughtful response to our article [1]. They present convincing data that excision of the β-toxin bacteriophage from Staphylococcus aureus strains does not contribute to host intracellular cytotoxicity. These data suggest that the increased virulence we observed in our animal models depends on extracellular effects of β-toxin. We agree with their analysis. Dupieux et al indicate that we suggested one mechanism of β-toxin involvement in virulence in vivo, namely its nucleoprotein CORRESPONDENCE
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Reply to Dupieux et al
ligase activity. This remains a viable possibility. However, we agree that there are multiple other possible mechanisms, including (1) the toxin’s ability to kill dividing immune cells, as noted by Huseby et al [2]; (2) altered immune system function, as a result of bioactivity of cleavage products from β-toxin sphingomyelinase activity at host plasma membranes; and (3) synergism with other cytotoxins. Note
Patrick Schlievert, Wilmara Salgado-Pabon, Alfa Herrera, Bao G. Vu, Christopher S. Stach, and Joseph A. Merriman Department of Microbiology, University of Iowa College of Medicine, Iowa City References 1. Salgado-Pabon W, Herrera A, Vu BG, et al. Staphylococcus aureus beta-toxin production is common in strains with the beta-toxin gene inactivated by bacteriophage. J Infect Dis 2014; 210:784–92. 2. Huseby MJ, Kruse AC, Digre J, et al. Beta toxin catalyzes formation of nucleoprotein matrix in staphylococcal biofilms. Proc Natl Acad Sci U S A 2010; 107:14407–12. Received 6 August 2014; accepted 19 August 2014; electronically published 1 September 2014. Correspondence: Patrick Schlievert, PhD, Department Microbiology, University of Iowa Carver College of Medicine, 51 Newton Rd, 3-403 Bowen Science Bldg, Iowa City, IA 52242 ([email protected]) The Journal of Infectious Diseases® 2015;211:847–8 © The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals. [email protected]. DOI: 10.1093/infdis/jiu495
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Potential conflicts of interest. All authors: No reported conflicts. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed
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JID 2015:211 (1 March)
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847
Downloaded from http://jid.oxfordjournals.org/ at University of California, San Francisco on April 7, 2015
Reply to Dupieux et al
ligase activity. This remains a viable possibility. However, we agree that there are multiple other possible mechanisms, including (1) the toxin’s ability to kill dividing immune cells, as noted by Huseby et al [2]; (2) altered immune system function, as a result of bioactivity of cleavage products from β-toxin sphingomyelinase activity at host plasma membranes; and (3) synergism with other cytotoxins. Note
Patrick Schlievert, Wilmara Salgado-Pabon, Alfa Herrera, Bao G. Vu, Christopher S. Stach, and Joseph A. Merriman Department of Microbiology, University of Iowa College of Medicine, Iowa City References 1. Salgado-Pabon W, Herrera A, Vu BG, et al. Staphylococcus aureus beta-toxin production is common in strains with the beta-toxin gene inactivated by bacteriophage. J Infect Dis 2014; 210:784–92. 2. Huseby MJ, Kruse AC, Digre J, et al. Beta toxin catalyzes formation of nucleoprotein matrix in staphylococcal biofilms. Proc Natl Acad Sci U S A 2010; 107:14407–12. Received 6 August 2014; accepted 19 August 2014; electronically published 1 September 2014. Correspondence: Patrick Schlievert, PhD, Department Microbiology, University of Iowa Carver College of Medicine, 51 Newton Rd, 3-403 Bowen Science Bldg, Iowa City, IA 52242 ([email protected]) The Journal of Infectious Diseases® 2015;211:847–8 © The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals. [email protected]. DOI: 10.1093/infdis/jiu495
848
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JID 2015:211 (1 March)
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CORRESPONDENCE
Downloaded from http://jid.oxfordjournals.org/ at University of California, San Francisco on April 7, 2015
Potential conflicts of interest. All authors: No reported conflicts. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed
