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  • American Society for Microbiology  (61)
  • 1
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    Maturation of Human Dendritic Cells by Cell Wall Skeleton of Mycobacterium bovis Bacillus Calmette-Guérin: Involvement of Toll-Like Receptors
    American Society for Microbiology ; 2000
    In:  Infection and Immunity Vol. 68, No. 12 ( 2000-12), p. 6883-6890
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 68, No. 12 ( 2000-12), p. 6883-6890
    Kurzfassung: The constituents of mycobacteria are an effective immune adjuvant, as observed with complete Freund's adjuvant. In this study, we demonstrated that the cell wall skeleton of Mycobacterium bovis bacillus Calmette-Guérin (BCG-CWS), a purified noninfectious material consisting of peptidoglycan, arabinogalactan, and mycolic acids, induces maturation of human dendritic cells (DC). Surface expression of CD40, CD80, CD83, and CD86 was increased by BCG-CWS on human immature DC, and the effect was similar to those of interleukin-1β (IL-1β), tumor necrosis factor alpha (TNF-α), heat-killed BCG, and viable BCG. BCG-CWS induced the secretion of TNF-α, IL-6, and IL-12 p40. CD83 expression was increased by a soluble factor secreted from BCG-CWS-treated DC and was completely inhibited by monoclonal antibodies against TNF-α. BCG-CWS-treated DC stimulated extensive allogeneic mixed lymphocyte reactions. The level of TNF-α secreted through BCG-CWS was partially suppressed in murine macrophages with no Toll-like receptor 2 (TLR 2) or TLR4 and was completely lost in TLR2 and TLR4 double-deficient macrophages. These results suggest that the BCG-CWS induces TNF-α secretion from DC via TLR2 and TLR4 and that the secreted TNF-α induces the maturation of DC per se.
    Materialart: Online-Ressource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.68.12.6883-6890.2000
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 2000
    ZDB Id: 1483247-1
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
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    Differential Role of MyD88 in Macrophage-Mediated Responses to Opportunistic Fungal Pathogens
    American Society for Microbiology ; 2003
    In:  Infection and Immunity Vol. 71, No. 9 ( 2003-09), p. 5280-5286
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 71, No. 9 ( 2003-09), p. 5280-5286
    Kurzfassung: Toll-like receptors mediate macrophage recognition of microbial ligands, inducing expression of microbicidal molecules and cytokines via the adapter protein MyD88. We investigated the role of MyD88 in regulating murine macrophage responses to a pathogenic yeast ( Candida albicans ) and mold ( Aspergillus fumigatus ). Macrophages derived from bone marrow of MyD88-deficient mice (MyD88 −/− ) demonstrated impaired phagocytosis and intracellular killing of C. albicans compared to wild-type (MyD88 +/+ ) macrophages. In contrast, ingestion and killing of A. fumigatus conidia was MyD88 independent. Cytokine production by MyD88 −/− macrophages in response to C. albicans yeasts and hyphae was substantially decreased, but responses to A. fumigatus hyphae were preserved. These results provide evidence that MyD88 signaling is involved in phagocytosis and killing of live C. albicans , but not A. fumigatus . The differential role of MyD88 may represent one mechanism by which macrophages regulate innate responses specific to different pathogenic fungi.
    Materialart: Online-Ressource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.71.9.5280-5286.2003
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 2003
    ZDB Id: 1483247-1
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
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    Differential Roles of Toll-Like Receptors 2 and 4 in In Vitro Responses of Macrophages to Legionella pneumophila
    American Society for Microbiology ; 2005
    In:  Infection and Immunity Vol. 73, No. 1 ( 2005-01), p. 352-361
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 73, No. 1 ( 2005-01), p. 352-361
    Kurzfassung: The role of Toll-like receptors (TLRs) in innate immunity to Legionella pneumophila , a gram-negative facultative intracellular bacterium, was studied by using bone marrow-derived macrophages and dendritic cells from TLR2-deficient (TLR2 −/− ), TLR4 −/− , and wild-type (WT) littermate (C57BL/6 × 129Sv) mice. Intracellular growth of L. pneumophila was enhanced within TLR2 −/− macrophages compared to WT and TLR4 −/− macrophages. There was no difference in the bacterial growth within dendritic cells from WT and TLR-deficient mice. Production of interleukin-12p40 (IL-12p40) and IL-10 after infection with L. pneumophila was attenuated in TLR2 −/− macrophages compared to WT and TLR4 −/− macrophages. Induction of IL-12p40, IL-10, and tumor necrosis factor alpha secretion from macrophages by the L. pneumophila dotO mutant, which cannot multiply within macrophages, and heat-killed bacteria, was similar to that caused by a viable virulent strain. There was no difference between the WT and its mutants in susceptibility to the cytopathic effect of bacteria. An L. pneumophila sonicated lysate induced IL-12p40 production by macrophages, but that of TLR2 −/− macrophages was significantly lower than those of WT and TLR4 −/− macrophages. Treatment of L. pneumophila sonicated lysate with proteinase K and heating did not abolish TLR2-dependent IL-12p40 production. Our results show that TLR2, but not TLR4, is involved in murine innate immunity against L. pneumophila , although other TLRs may also contribute to innate immunity against this organism.
    Materialart: Online-Ressource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.73.1.352-361.2005
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 2005
    ZDB Id: 1483247-1
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
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    USP15 Participates in Hepatitis C Virus Propagation through Regulation of Viral RNA Translation and Lipid Droplet Formation
    American Society for Microbiology ; 2019
    In:  Journal of Virology Vol. 93, No. 6 ( 2019-03-15)
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 93, No. 6 ( 2019-03-15)
    Kurzfassung: Hepatitis C virus (HCV) utilizes cellular factors for efficient propagation. Ubiquitin is covalently conjugated to the substrate to alter its stability or to modulate signal transduction. In this study, we examined the importance of ubiquitination for HCV propagation. We found that inhibition of deubiquitinating enzymes (DUBs) or overexpression of nonspecific DUBs impaired HCV replication, suggesting that ubiquitination regulates HCV replication. To identify specific DUBs involved in HCV propagation, we set up RNA interference (RNAi) screening against DUBs and successfully identified ubiquitin-specific protease 15 (USP15) as a novel host factor for HCV propagation. Our studies showed that USP15 is involved in translation of HCV RNA and production of infectious HCV particles. In addition, deficiency of USP15 in human hepatic cell lines (Huh7 and Hep3B/miR-122 cells) but not in a nonhepatic cell line (293T cells) impaired HCV propagation, suggesting that USP15 participates in HCV propagation through the regulation of hepatocyte-specific functions. Moreover, we showed that loss of USP15 had no effect on innate immune responses in vitro and in vivo . We also found that USP15-deficient Huh7 cells showed reductions in the amounts of lipid droplets (LDs), and the addition of palmitic acids restored the production of infectious HCV particles. Taken together, these data suggest that USP15 participates in HCV propagation by regulating the translation of HCV RNA and the formation of LDs. IMPORTANCE Although ubiquitination has been shown to play important roles in the HCV life cycle, the roles of deubiquitinating enzymes (DUBs), which cleave ubiquitin chains from their substrates, in HCV propagation have not been investigated. Here, we identified USP15 as a DUB regulating HCV propagation. USP15 showed no interaction with viral proteins and no participation in innate immune responses. Deficiency of USP15 in Huh7 cells resulted in suppression of the translation of HCV RNA and reduction in the amounts of lipid droplets, and the addition of fatty acids partially restored the production of infectious HCV particles. These data suggest that USP15 participates in HCV propagation in hepatic cells through the regulation of viral RNA translation and lipid metabolism.
    Materialart: Online-Ressource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.01708-18
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 2019
    ZDB Id: 1495529-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
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    Distinct Roles for MyD88 and Toll-Like Receptors 2, 5, and 9 in Phagocytosis of Borrelia burgdorferi and Cytokine Induction
    American Society for Microbiology ; 2008
    In:  Infection and Immunity Vol. 76, No. 6 ( 2008-06), p. 2341-2351
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 76, No. 6 ( 2008-06), p. 2341-2351
    Kurzfassung: The contribution of Toll-like receptors (TLRs) to phagocytosis of Borrelia burgdorferi has not been extensively studied. We show that bone marrow-derived macrophages (BMDM) from MyD88 −/− mice or Raw cells transfected with a dominant-negative MyD88 were unable to efficiently internalize B. burgdorferi. Knockouts of TLR2 and TLR9 or knockdown of TLR5 by small interfering RNA produced no defects in phagocytosis of B. burgdorferi . Production of inflammatory cytokines was greatly diminished in MyD88 −/− BMDM but only partially affected in TLR2 −/− BMDM or knockdown of TLR5 and unaffected in TLR9 −/− BMDM. Cytochalasin D reduced cytokine induction, but not to the level of the MyD88 −/− BMDM. Addition of cytochalasin D to TLR2 −/− BMDM inhibited inflammatory responses to B. burgdorferi to the level of MyD88 −/− BMDM, consistent with a role for TLR2 in both recognition of extracellular products and lysosomal sampling by TLR2 after processing of the organism. Cytochalasin D had no impact on cytokine production in cells undergoing TLR5 knockdown. These results suggest that MyD88, but not TLR2, TLR5, and TLR9, is important for the uptake of B. burgdorferi and that MyD88 affects inflammatory responses through both its effects on phagocytosis and its role in transducing signals from TLR2 and TLR5.
    Materialart: Online-Ressource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.01600-07
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 2008
    ZDB Id: 1483247-1
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
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    Interleukin-18 Impairs the Pulmonary Host Response to Pseudomonas aeruginosa
    American Society for Microbiology ; 2003
    In:  Infection and Immunity Vol. 71, No. 4 ( 2003-04), p. 1630-1634
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 71, No. 4 ( 2003-04), p. 1630-1634
    Kurzfassung: Interleukin-18 (IL-18) is a potent cytokine with many different proinflammatory activities. To study the role of IL-18 in the pathogenesis of Pseudomonas pneumonia, IL-18-deficient ( IL-18 −/− ) and wild-type mice were intranasally inoculated with Pseudomonas aeruginosa . IL-18 deficiency was associated with reduced outgrowth of Pseudomonas in the lungs and diminished dissemination of the infection. In addition, pulmonary inflammation (histopathology) and levels of tumor necrosis factor alpha, IL-6, and macrophage inflammatory protein-2 in lungs and plasma were lower in IL-18 −/− mice. Consistent with results obtained for IL-18 −/− mice, treatment of wild-type mice with a neutralizing IL-18 binding protein-immunoglobulin G Fc fusion construct also attenuated outgrowth of Pseudomonas compared with that for mice treated with a control protein. These results demonstrate that the presence of endogenous IL-18 activity facilitates inflammatory responses in the lung during Pseudomonas pneumonia, concurrently impairing bacterial clearance.
    Materialart: Online-Ressource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.71.4.1630-1634.2003
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 2003
    ZDB Id: 1483247-1
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 7
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    Role of Adrenomedullin in Lyme Disease
    American Society for Microbiology ; 2010
    In:  Infection and Immunity Vol. 78, No. 12 ( 2010-12), p. 5307-5313
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 78, No. 12 ( 2010-12), p. 5307-5313
    Kurzfassung: Borrelia burgdorferi stimulates a strong inflammatory response during infection of a mammalian host. To understand the mechanisms of immune regulation employed by the host to control this inflammatory response, we focused our studies on adrenomedullin, a peptide produced in response to bacterial stimuli that exhibits antimicrobial activity and regulates inflammatory responses by modulating the expression of inflammatory cytokines. Specifically, we investigated the effect of B. burgdorferi on the expression of adrenomedullin as well as the ability of adrenomedullin to dampen host inflammatory responses to the spirochete. The concentration of adrenomedullin in the synovial fluid of untreated Lyme arthritis patients was elevated compared with that in control osteoarthritis patient samples. In addition, coculture with B. burgdorferi significantly increased the expression of adrenomedullin in RAW264.7 macrophages through MyD88-, phosphatidylinositol 3-kinase (PI3-K)-, and p38-dependent signaling cascades. Furthermore, the addition of exogenous adrenomedullin to B. burgdorferi- stimulated RAW264.7 macrophages resulted in a significant decrease in the induction of proinflammatory cytokines. Taken together, these results suggest that B. burgdorferi increases the production of adrenomedullin, which in turn negatively regulates the B. burgdorferi- stimulated inflammatory response.
    Materialart: Online-Ressource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.00630-10
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 2010
    ZDB Id: 1483247-1
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 8
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    Dual Role of MyD88 in Rapid Clearance of Relapsing Fever Borrelia spp
    American Society for Microbiology ; 2006
    In:  Infection and Immunity Vol. 74, No. 12 ( 2006-12), p. 6750-6760
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 74, No. 12 ( 2006-12), p. 6750-6760
    Kurzfassung: Relapsing fever Borrelia spp. undergo antigenic variation, achieve high levels in blood, and require rapid production of immunoglobulin M (IgM) for clearance. MyD88-deficient mice display defective clearance of many pathogens; however, the IgM response to persistent infection is essentially normal. Therefore, MyD88 −/− mice provided a unique opportunity to study the effect of nonantibody, innate host defenses to relapsing fever Borrelia . Infected MyD88 −/− mice harbored extremely high levels of B. hermsii in the blood compared to wild-type littermates. In the comparison of MyD88 −/− mice and B- and T-cell-deficient scid mice, two features stood out: (i) bacterial numbers in blood were at least 10-fold greater in MyD88 −/− mice than scid mice, even though the production of IgM still occurred in MyD88 −/− mice; and (ii) many of the MyD88 −/− mice were able to exert partial clearance, although with delayed kinetics relative to wild-type mice, a feature not seen in scid mice. Further analysis revealed a delay in the IgM response to lipoproteins expressed by the original inoculum; however, by 6 days of infection antibodies were produced in MyD88 −/− mice that could clear spirochetemia in scid mice. While these results indicated that the production of IgM was delayed in MyD88 −/− mice, they also point to a second, antibody-independent role for MyD88 signaling in host defense to relapsing fever Borrelia . This second defect was apparent only when antibody levels were limiting.
    Materialart: Online-Ressource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.01160-06
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 2006
    ZDB Id: 1483247-1
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 9
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    Toll-Like Receptor 4 Mediates Tolerance in Macrophages Stimulated with Toxoplasma gondii- Derived Heat Shock Protein 70
    American Society for Microbiology ; 2005
    In:  Infection and Immunity Vol. 73, No. 8 ( 2005-08), p. 4634-4642
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 73, No. 8 ( 2005-08), p. 4634-4642
    Kurzfassung: Peritoneal macrophages (PMs) from toll-like receptor 4 (TLR4)-deficient and wild-type (WT) mice were responsive to recombinant Toxoplasma gondii -derived heat shock protein 70 (rTgHSP70) and natural TgHSP70 (nTgHSP70) in NO release, but those from TLR2-, myeloid differentiation factor 88 (MyD88)-, and interleukin-1R-associated kinase 4 (IRAK4)-deficient mice were not. Polymyxin B did not inhibit PM activation by TgHSP70 and nTgHSP70 from WT and TLR4-deficient mice, while it inhibited PM activation by lipopolysaccharide. Pretreatment of PMs from WT but not from TLR4-deficient mice with rTgHSP70 resulted in suppression of NO release on restimulation with rTgHSP70. Similarly, pretreatment of PMs from WT but not TLR4-deficient mice with nTgHSP70 resulted in suppression of NO release on restimulation with nTgHSP70. Polymyxin B did not inhibit rTgHSP70- and nTgHSP70-induced tolerance of PMs from TLR4-deficient mice. Furthermore, PMs from WT mice increased suppressor of cytokine-signaling-1 (SOCS-1) expression after restimulation with rTgHSP70, while those from TLR4-deficient mice did not. Phosphorylation of JNK and I-κBα occurred in rTgHSP70-induced tolerance of PMs from TLR4-deficient mice, but not in that from WT mice. These data indicated that TgHSP70 signaling mechanisms were mediated by TLR2, MyD88, and IRAK4, but not by TLR4. On the other hand, signaling of TgHSP70-induced tolerance was mediated by TLR4, and the expression of SOCS-1 suppressed the TLR2 signaling pathway.
    Materialart: Online-Ressource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.73.8.4634-4642.2005
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 2005
    ZDB Id: 1483247-1
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 10
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    Papillomavirus Capsid Mutation To Escape Dendritic Cell-Dependent Innate Immunity in Cervical Cancer
    American Society for Microbiology ; 2005
    In:  Journal of Virology Vol. 79, No. 11 ( 2005-06), p. 6741-6750
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 79, No. 11 ( 2005-06), p. 6741-6750
    Kurzfassung: Infection with oncogenic human papillomaviruses (HPVs), typified by HPV type 16 (HPV16), is a necessary cause of cervical cancer. Prophylactic vaccination with HPV16 L1 virus-like particles (VLPs) provides immunity. HPV16 VLPs activate dendritic cells and a potent neutralizing immunoglobulin G (IgG) response, yet many cervical cancer patients fail to generate detectable VLP-specific IgG. Therefore, we examined the role of the innate recognition of HPV16 L1 in VLP-induced immune responses and its evasion during carcinogenesis. Nonconservative mutations within HPV16 L1 have been described in isolates from cervical cancer and its precursor, high-grade cervical intraepithelial neoplasia (CIN). We determined the effect of mutations in L1 upon in vitro self-assembly into VLPs and their influence upon the induction of innate and adaptive immune responses in mice. Several nonconservative mutations in HPV16 L1 isolated from high-grade CIN or cervical carcinoma prevent self-assembly of L1 VLPs. Intact VLPs, but not assembly-defective L1, activate dendritic cells to produce proinflammatory factors, such as alpha interferon, that play a critical role in inducing adaptive immunity. Indeed, effective induction of L1-specific IgG1 and IgG2a was dependent upon intact VLP structure. Dendritic cell activation and production of virus-specific neutralizing IgG by VLPs requires MyD88-dependent signaling, although the L1 structure that initiates MyD88-mediated signaling is distinct from the neutralizing epitopes. We conclude that innate recognition of the intact L1 VLP structure via MyD88 is critical in the induction of high-titer neutralizing IgG. Tumor progression is associated with genetic instability and L1 mutants. Selection for assembly-deficient L1 mutations suggests the evasion of MyD88-dependent immune control during cervical carcinogenesis.
    Materialart: Online-Ressource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.79.11.6741-6750.2005
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 2005
    ZDB Id: 1495529-5
    Standort Signatur Einschränkungen Verfügbarkeit
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