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  1. Article: Epithelial cell signaling responses to enterohemorrhagic Escherichia coli infection.

    Ceponis, Peter J M / Riff, Jason D / Sherman, Philip M

    Memorias do Instituto Oswaldo Cruz

    2005  Volume 100 Suppl 1, Page(s) 199–203

    Abstract: Enterohemorrhagic Escherichia coli, including the serotype O157:H7 that is most commonly identified with human disease, cause both sporadic cases and outbreaks of non-bloody diarrhea and hemorrhagic colitis. In about 10% of infected subjects, the ... ...

    Abstract Enterohemorrhagic Escherichia coli, including the serotype O157:H7 that is most commonly identified with human disease, cause both sporadic cases and outbreaks of non-bloody diarrhea and hemorrhagic colitis. In about 10% of infected subjects, the hemolytic uremic syndrome (hemolytic anemic, thrombocytopenia, and acute renal failure) develops, likely as a consequence of systemic spread of bacterial-derived toxins variously referred to as Shiga-like toxin, Shiga toxin, and Verotoxin. Increasing evidence points to a complex interplay between bacterial products--for example, adhesins and toxins--and host signal transduction pathways in mediating responses to infection. Identification of critical signaling pathways could result in the development of novel strategies for intervention to both prevent and treat this microbial infection in humans.
    MeSH term(s) Animals ; Apoptosis/physiology ; Epithelial Cells/microbiology ; Epithelial Cells/physiology ; Escherichia coli Infections/microbiology ; Escherichia coli O157/pathogenicity ; Gastrointestinal Hemorrhage/microbiology ; Humans ; STAT1 Transcription Factor/metabolism ; Signal Transduction/physiology
    Chemical Substances STAT1 Transcription Factor ; STAT1 protein, human
    Language English
    Publishing date 2005-06-14
    Publishing country Brazil
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 953293-6
    ISSN 1678-8060 ; 0074-0276
    ISSN (online) 1678-8060
    ISSN 0074-0276
    DOI 10.1590/s0074-02762005000900034
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Cholesterol-enriched membrane microdomains are required for inducing host cell cytoskeleton rearrangements in response to attaching-effacing Escherichia coli.

    Riff, Jason D / Callahan, John W / Sherman, Philip M

    Infection and immunity

    2005  Volume 73, Issue 11, Page(s) 7113–7125

    Abstract: The diarrheal pathogens enterohemorrhagic Escherichia coli (EHEC) O157:H7 strain CL56 and enteropathogenic Escherichia coli (EPEC) O127:H6 strain E2348/69 adhere intimately to epithelial cells through attaching-effacing lesions, which are characterized ... ...

    Abstract The diarrheal pathogens enterohemorrhagic Escherichia coli (EHEC) O157:H7 strain CL56 and enteropathogenic Escherichia coli (EPEC) O127:H6 strain E2348/69 adhere intimately to epithelial cells through attaching-effacing lesions, which are characterized by rearrangements of the host cytoskeleton, intimate adherence, and destruction of microvilli. These cytoskeletal responses require activation of host signal transduction pathways. Lipid rafts are signaling microdomains enriched in sphingolipid and cholesterol in the plasma membrane. The effect of perturbing plasma membrane cholesterol on bacterial intimate adherence was assessed. Infection of both HEp-2 cells and primary skin fibroblasts with strains CL56 and E2348/69 caused characteristic rearrangements of the cytoskeleton at sites of bacterial adhesion. CL56- and E2348/69-induced cytoskeletal rearrangements were inhibited following cholesterol depletion. Addition of exogenous cholesterol to depleted HEp-2 cells restored cholesterol levels and rescued bacterially induced alpha-actinin mobilization. Quantitative bacterial adherence assays showed that EPEC adherence to HEp-2 cells was dramatically reduced following cholesterol depletion, whereas the adherence of EHEC remained high. Cytoskeletal rearrangements on skin fibroblasts obtained from children with Niemann-Pick type C disease were markedly reduced. These findings indicate that host membrane cholesterol contained in lipid rafts is necessary for the cytoskeletal rearrangements following infection with attaching-effacing Escherichia coli. Differences in initial adherence indicate divergent roles for host membrane cholesterol in the pathogenesis of EHEC and EPEC infections.
    MeSH term(s) Actinin/metabolism ; Adhesins, Bacterial/metabolism ; Bacterial Adhesion ; Cell Line ; Cholesterol/metabolism ; Cytoskeleton/metabolism ; Epithelial Cells/cytology ; Epithelial Cells/metabolism ; Epithelial Cells/microbiology ; Epithelial Cells/ultrastructure ; Escherichia coli O157/physiology ; Escherichia coli Proteins/metabolism ; Humans ; Membrane Microdomains/chemistry ; Membrane Microdomains/metabolism ; beta-Cyclodextrins/pharmacology
    Chemical Substances Adhesins, Bacterial ; Escherichia coli Proteins ; beta-Cyclodextrins ; methyl-beta-cyclodextrin ; Actinin (11003-00-2) ; eaeA protein, E coli (147094-99-3) ; Cholesterol (97C5T2UQ7J)
    Language English
    Publishing date 2005-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218698-6
    ISSN 1098-5522 ; 0019-9567
    ISSN (online) 1098-5522
    ISSN 0019-9567
    DOI 10.1128/IAI.73.11.7113-7125.2005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 684: Show issues Location:
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  3. Article: Cholesterol-Enriched Membrane Microdomains Are Required for Inducing Host Cell Cytoskeleton Rearrangements in Response to Attaching-Effacing Escherichia coli

    Riff, Jason D / Callahan, John W / Sherman, Philip M

    Infection and immunity. 2005 Nov., v. 73, no. 11

    2005  

    Abstract: The diarrheal pathogens enterohemorrhagic Escherichia coli (EHEC) O157:H7 strain CL56 and enteropathogenic Escherichia coli (EPEC) O127:H6 strain E2348/69 adhere intimately to epithelial cells through attaching-effacing lesions, which are characterized ... ...

    Abstract The diarrheal pathogens enterohemorrhagic Escherichia coli (EHEC) O157:H7 strain CL56 and enteropathogenic Escherichia coli (EPEC) O127:H6 strain E2348/69 adhere intimately to epithelial cells through attaching-effacing lesions, which are characterized by rearrangements of the host cytoskeleton, intimate adherence, and destruction of microvilli. These cytoskeletal responses require activation of host signal transduction pathways. Lipid rafts are signaling microdomains enriched in sphingolipid and cholesterol in the plasma membrane. The effect of perturbing plasma membrane cholesterol on bacterial intimate adherence was assessed. Infection of both HEp-2 cells and primary skin fibroblasts with strains CL56 and E2348/69 caused characteristic rearrangements of the cytoskeleton at sites of bacterial adhesion. CL56- and E2348/69-induced cytoskeletal rearrangements were inhibited following cholesterol depletion. Addition of exogenous cholesterol to depleted HEp-2 cells restored cholesterol levels and rescued bacterially induced [alpha]-actinin mobilization. Quantitative bacterial adherence assays showed that EPEC adherence to HEp-2 cells was dramatically reduced following cholesterol depletion, whereas the adherence of EHEC remained high. Cytoskeletal rearrangements on skin fibroblasts obtained from children with Niemann-Pick type C disease were markedly reduced. These findings indicate that host membrane cholesterol contained in lipid rafts is necessary for the cytoskeletal rearrangements following infection with attaching-effacing Escherichia coli. Differences in initial adherence indicate divergent roles for host membrane cholesterol in the pathogenesis of EHEC and EPEC infections.
    Keywords bacterial adhesion ; children ; cholesterol ; cytoskeleton ; enterohemorrhagic Escherichia coli ; enteropathogenic Escherichia coli ; epithelial cells ; fibroblasts ; human cell lines ; microvilli ; pathogenesis ; pathogens ; plasma membrane ; signal transduction ; sphingolipids
    Language English
    Size p. 7113-7125.
    Publishing place American Society for Microbiology
    Document type Article
    ZDB-ID 218698-6
    ISSN 1098-5522 ; 0019-9567
    ISSN (online) 1098-5522
    ISSN 0019-9567
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 684: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  4. Article: Conditioned Medium from Enterohemorrhagic Escherichia coli-Infected T84 Cells Inhibits Signal Transducer and Activator of Transcription 1 Activation by Gamma Interferon

    Jandu, Narveen / Ceponis, Peter J. M / Kato, Seiichi / Riff, Jason D / McKay, Derek M / Sherman, Philip M

    Infection and immunity. 2006 Mar., v. 74, no. 3

    2006  

    Abstract: Gamma interferon (IFN-[gamma]) is a cytokine important to host defense which can signal through signal transducer and activator of transcription 1 (Stat1). Enterohemorrhagic Escherichia coli (EHEC) modulates host cell signal transduction to establish ... ...

    Abstract Gamma interferon (IFN-[gamma]) is a cytokine important to host defense which can signal through signal transducer and activator of transcription 1 (Stat1). Enterohemorrhagic Escherichia coli (EHEC) modulates host cell signal transduction to establish infection, and EHEC serotypes O113:H21 and O157:H7 both inhibit IFN-[gamma]-induced Stat1 tyrosine phosphorylation in vitro. The aim of this study was to delineate both bacterial and host cell factors involved in the inhibition of Stat1 tyrosine phosphorylation. Human T84 colonic epithelial cells were challenged with direct infection, viable EHEC separated from T84 cells by a filter, sodium orthovanadate, isolated flagellin, bacterial culture supernatants, and conditioned medium treated with proteinase K, trypsin, or heat inactivation. Epithelial cells were then stimulated with IFN-[gamma] and protein extracts were analyzed by immunoblotting. The data showed that IFN-[gamma]-inducible Stat1 tyrosine phosphorylation was inhibited when EHEC adhered to T84 cells, but not by bacterial culture supernatants or bacteria separated from the epithelial monolayer. Conditioned medium from T84 cells infected with EHEC O157:H7 suppressed Stat1 activation, and this was not reversed by treatment with proteinases or heat inactivation. Use of pharmacological inhibitors showed that time-dependent bacterial, but not epithelial, protein synthesis was involved. Stat1 inhibition was also independent of bacterial flagellin, host proteasome activity, and protein tyrosine phosphatases. Infection led to altered IFN-[gamma] receptor domain 1 subcellular distribution and decreased expression in cholesterol-enriched membrane microdomains. Thus, suppression of host cell IFN-[gamma] signaling by production of a contact-dependent, soluble EHEC factor may represent a novel mechanism for this pathogen to evade the host immune system.
    Keywords bacteria ; enterohemorrhagic Escherichia coli ; epithelial cells ; flagellin ; heat inactivation ; humans ; immune system ; immunoblotting ; interferon-gamma ; pathogens ; peptidase K ; phosphorylation ; proteasome endopeptidase complex ; protein synthesis ; protein-tyrosine-phosphatase ; serotypes ; signal transduction ; transcription factors ; trypsin ; tyrosine
    Language English
    Size p. 1809-1818.
    Publishing place American Society for Microbiology
    Document type Article
    ZDB-ID 218698-6
    ISSN 1098-5522 ; 0019-9567
    ISSN (online) 1098-5522
    ISSN 0019-9567
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 684: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  5. Article: Conditioned medium from enterohemorrhagic Escherichia coli-infected T84 cells inhibits signal transducer and activator of transcription 1 activation by gamma interferon.

    Jandu, Narveen / Ceponis, Peter J M / Kato, Seiichi / Riff, Jason D / McKay, Derek M / Sherman, Philip M

    Infection and immunity

    2006  Volume 74, Issue 3, Page(s) 1809–1818

    Abstract: Gamma interferon (IFN-gamma) is a cytokine important to host defense which can signal through signal transducer and activator of transcription 1 (Stat1). Enterohemorrhagic Escherichia coli (EHEC) modulates host cell signal transduction to establish ... ...

    Abstract Gamma interferon (IFN-gamma) is a cytokine important to host defense which can signal through signal transducer and activator of transcription 1 (Stat1). Enterohemorrhagic Escherichia coli (EHEC) modulates host cell signal transduction to establish infection, and EHEC serotypes O113:H21 and O157:H7 both inhibit IFN-gamma-induced Stat1 tyrosine phosphorylation in vitro. The aim of this study was to delineate both bacterial and host cell factors involved in the inhibition of Stat1 tyrosine phosphorylation. Human T84 colonic epithelial cells were challenged with direct infection, viable EHEC separated from T84 cells by a filter, sodium orthovanadate, isolated flagellin, bacterial culture supernatants, and conditioned medium treated with proteinase K, trypsin, or heat inactivation. Epithelial cells were then stimulated with IFN-gamma and protein extracts were analyzed by immunoblotting. The data showed that IFN-gamma-inducible Stat1 tyrosine phosphorylation was inhibited when EHEC adhered to T84 cells, but not by bacterial culture supernatants or bacteria separated from the epithelial monolayer. Conditioned medium from T84 cells infected with EHEC O157:H7 suppressed Stat1 activation, and this was not reversed by treatment with proteinases or heat inactivation. Use of pharmacological inhibitors showed that time-dependent bacterial, but not epithelial, protein synthesis was involved. Stat1 inhibition was also independent of bacterial flagellin, host proteasome activity, and protein tyrosine phosphatases. Infection led to altered IFN-gamma receptor domain 1 subcellular distribution and decreased expression in cholesterol-enriched membrane microdomains. Thus, suppression of host cell IFN-gamma signaling by production of a contact-dependent, soluble EHEC factor may represent a novel mechanism for this pathogen to evade the host immune system.
    MeSH term(s) Culture Media, Conditioned/pharmacology ; Drug Interactions ; Epithelial Cells/metabolism ; Escherichia coli Infections/metabolism ; Escherichia coli Infections/physiopathology ; Escherichia coli O157/physiology ; Interferon-gamma/pharmacology ; STAT1 Transcription Factor/antagonists & inhibitors ; STAT1 Transcription Factor/metabolism ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Trans-Activators/metabolism
    Chemical Substances Culture Media, Conditioned ; STAT1 Transcription Factor ; STAT1 protein, human ; Trans-Activators ; Interferon-gamma (82115-62-6)
    Language English
    Publishing date 2006-03
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218698-6
    ISSN 1098-5522 ; 0019-9567
    ISSN (online) 1098-5522
    ISSN 0019-9567
    DOI 10.1128/IAI.74.3.1809-1818.2006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 684: Show issues Location:
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