CORRECTION article

Front. Microbiol., 19 October 2018

Sec. Antimicrobials, Resistance and Chemotherapy

Volume 9 - 2018 | https://doi.org/10.3389/fmicb.2018.02511

Corrigendum: Staphylococcus aureus Bacteriophage Suppresses LPS-Induced Inflammation in MAC-T Bovine Mammary Epithelial Cells

    LZ

    Lili Zhang

    XH

    Xiang Hou

    LS

    Lichang Sun

    TH

    Tao He

    RW

    Ruicheng Wei

    MP

    Maoda Pang

    RW

    Ran Wang *

  • Key Laboratory of Food Quality and Safety of Jiangsu Province-State Key Laboratory Breeding Base, Institute of Food Safety and Nutrition, Jiangsu Academy of Agricultural Sciences, Nanjing, China

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In the original article, there was an error. We stated in the article that Previous studies reported that bacteriophages could activate NF-κB signaling and enhance immune effects in vitro (Gorski et al., 2006). In fact, the authors of the aforementioned article reported the exact opposite; that is, they reported a phage-mediated down-regulation of NF-κB activation.

A correction has been made to Discussion, Paragraph 3:

Previous studies reported that bacteriophages can diminish cellular infiltration of allogeneic skin allograft in mice, extend its survival and inhibit human T cell activation in vitro. Furthermore, T4 phage can abolish the ability of the pathogenic virus to induce NF-κB activity (Gorski et al., 2006). In order to prove the relationship between the effects induced by bacteriophages and NF-κB, we determined the expression levels and the phosphorylation of the NF-κB p65 subunit were determined by Western blotting. This part of our work demonstrated that pre-treatment with bacteriophage vB_SauM_JS25 significantly suppressed the phosphorylation levels of NF-κB p65 at 2 h post-LPS-stimulation (p < 0.05, Figure 4). However, once the pre-treatment bacteriophage was removed, the LPS-induced production of cytokines was significantly enhanced (p < 0.001, Figure 3). As reported previously, the lack of dissemination, and the reduced levels of inflammation caused by the production of prophage-created conditions, could promote persistent infection by P. aeruginosa (Secor et al., 2017). Moreover, there may be other mechanisms that bacteriophages use to interact directly with eukaryotic systems and thus modulate the immune system. In these scenarios, bacteriophages appear to act an immunomodulator in order to balance inflammation cytokines.

The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way.

The original article has been updated.

Statements

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

References

  • 1

    GorskiA.KniotekM.Perkowska-PtasinskaA.MrozA.PrzerwaA.GorczycaW.et al. (2006). Bacteriophages and transplantation tolerance. Transplant. Proc.38, 331333. 10.1016/j.transproceed.2005.12.073

  • 2

    SecorP. R.MichaelsL. A.SmigielK. S.RohaniM. G.JenningsL. K.HisertK. B.et al. (2017). Filamentous bacteriophage produced by Pseudomonas aeruginosa alters the inflammatory response and promotes noninvasive infection in vivo. Infect. Immun. 85:e0064816. 10.1128/IAI.00648-16

Summary

Keywords

Staphylococcus aureus, bacteriophage, inflammation, LPS, NF-κB, MAC-T cells

Citation

Zhang L, Hou X, Sun L, He T, Wei R, Pang M and Wang R (2018) Corrigendum: Staphylococcus aureus Bacteriophage Suppresses LPS-Induced Inflammation in MAC-T Bovine Mammary Epithelial Cells. Front. Microbiol. 9:2511. doi: 10.3389/fmicb.2018.02511

Received

02 August 2018

Accepted

02 October 2018

Published

19 October 2018

Volume

9 - 2018

Edited by

Pilar García, Consejo Superior de Investigaciones Científicas (CSIC), Spain

Reviewed by

Andrzej Gorski, Ludwik Hirszfeld Institute of Immunology and Experimental Therapy (PAN), Poland

Updates

Copyright

*Correspondence: Ran Wang

This article was submitted to Antimicrobials, Resistance and Chemotherapy, a section of the journal Frontiers in Microbiology

Disclaimer

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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