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  1. Article ; Online: Corrigendum: Heterogeneous Family of Cyclomodulins: Smart Weapons That Allow Bacteria to Hijack the Eukaryotic Cell Cycle and Promote Infections.

    El-Aouar Filho, Rachid A / Nicolas, Aurélie / De Paula Castro, Thiago L / Deplanche, Martine / De Carvalho Azevedo, Vasco A / Goossens, Pierre L / Taieb, Frédéric / Lina, Gerard / Le Loir, Yves / Berkova, Nadia

    Frontiers in cellular and infection microbiology

    2017  Volume 7, Page(s) 364

    Abstract: This corrects the article on p. 208 in vol. 7, PMID: 28589102.]. ...

    Abstract [This corrects the article on p. 208 in vol. 7, PMID: 28589102.].
    Language English
    Publishing date 2017-08-14
    Publishing country Switzerland
    Document type Published Erratum
    ZDB-ID 2619676-1
    ISSN 2235-2988 ; 2235-2988
    ISSN (online) 2235-2988
    ISSN 2235-2988
    DOI 10.3389/fcimb.2017.00364
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Heterogeneous Family of Cyclomodulins: Smart Weapons That Allow Bacteria to Hijack the Eukaryotic Cell Cycle and Promote Infections.

    El-Aouar Filho, Rachid A / Nicolas, Aurélie / De Paula Castro, Thiago L / Deplanche, Martine / De Carvalho Azevedo, Vasco A / Goossens, Pierre L / Taieb, Frédéric / Lina, Gerard / Le Loir, Yves / Berkova, Nadia

    Frontiers in cellular and infection microbiology

    2017  Volume 7, Page(s) 208

    Abstract: Some bacterial pathogens modulate signaling pathways of eukaryotic cells in order to subvert the host response for their own benefit, leading to successful colonization and invasion. Pathogenic bacteria produce multiple compounds that generate favorable ... ...

    Abstract Some bacterial pathogens modulate signaling pathways of eukaryotic cells in order to subvert the host response for their own benefit, leading to successful colonization and invasion. Pathogenic bacteria produce multiple compounds that generate favorable conditions to their survival and growth during infection in eukaryotic hosts. Many bacterial toxins can alter the cell cycle progression of host cells, impairing essential cellular functions and impeding host cell division. This review summarizes current knowledge regarding cyclomodulins, a heterogeneous family of bacterial effectors that induce eukaryotic cell cycle alterations. We discuss the mechanisms of actions of cyclomodulins according to their biochemical properties, providing examples of various cyclomodulins such as cycle inhibiting factor, γ-glutamyltranspeptidase, cytolethal distending toxins, shiga toxin, subtilase toxin, anthrax toxin, cholera toxin, adenylate cyclase toxins, vacuolating cytotoxin, cytotoxic necrotizing factor, Panton-Valentine leukocidin, phenol soluble modulins, and mycolactone. Special attention is paid to the benefit provided by cyclomodulins to bacteria during colonization of the host.
    Language English
    Publishing date 2017
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2619676-1
    ISSN 2235-2988 ; 2235-2988
    ISSN (online) 2235-2988
    ISSN 2235-2988
    DOI 10.3389/fcimb.2017.00208
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Phenol-soluble modulin α induces G2/M phase transition delay in eukaryotic HeLa cells.

    Deplanche, Martine / Filho, Rachid Aref El-Aouar / Alekseeva, Ludmila / Ladier, Emilie / Jardin, Julien / Henry, Gwénaële / Azevedo, Vasco / Miyoshi, Anderson / Beraud, Laetitia / Laurent, Frederic / Lina, Gerard / Vandenesch, François / Steghens, Jean-Paul / Le Loir, Yves / Otto, Michael / Götz, Friedrich / Berkova, Nadia

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2015  Volume 29, Issue 5, Page(s) 1950–1959

    Abstract: Staphylococcus aureus is a gram-positive bacterium responsible for a wide range of infections. Host cell cycle alteration is a sophisticated mechanism used by pathogens to hijack the defense functions of host cells. We previously demonstrated that S. ... ...

    Abstract Staphylococcus aureus is a gram-positive bacterium responsible for a wide range of infections. Host cell cycle alteration is a sophisticated mechanism used by pathogens to hijack the defense functions of host cells. We previously demonstrated that S. aureus MW2 (USA400) bacteria induced a G2/M phase transition delay in HeLa cells. We demonstrate here that this activity is triggered by culture supernatant compounds. Using size exclusion chromatography of the MW2 supernatant, followed by mass spectroscopy analysis of corresponding peaks, we identified phenol-soluble modulin α (PSMα) peptides as the likely candidates for this effect. Indeed, synthetic PSMα1 and PSMα3 caused a G2/M phase transition delay. The implication of PSMα in cell cycle alteration was confirmed by comparison of S. aureus Los Angeles County clone (LAC) wild-type with the isogenic mutant LAC∆psmα, which lacks the psmα operon encoding PSMα1-4. PSMα-induced G2/M transition delay correlated with a decrease in the defensin genes expression suggesting a diminution of antibacterial functions of epithelial cells. By testing the supernatant of S. aureus human clinical isolates, we found that the degree of G2/M phase transition delay correlated with PSMα1 production. We show that PSMs secreted by S. aureus alter the host cell cycle, revealing a newly identified mechanism for fostering an infection.
    MeSH term(s) Bacterial Toxins/pharmacology ; Blotting, Western ; Cell Proliferation ; Cells, Cultured ; Culture Media, Conditioned/pharmacology ; Flow Cytometry ; G2 Phase Cell Cycle Checkpoints/drug effects ; HeLa Cells ; Humans ; M Phase Cell Cycle Checkpoints/drug effects ; Peptide Fragments/pharmacology ; Phenol/chemistry ; Staphylococcal Infections/microbiology ; Staphylococcus aureus/physiology ; Tandem Mass Spectrometry
    Chemical Substances Bacterial Toxins ; Culture Media, Conditioned ; Peptide Fragments ; Phenol (339NCG44TV)
    Language English
    Publishing date 2015-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.14-260513
    Database MEDical Literature Analysis and Retrieval System OnLINE

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