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  • Medicine  (3)
  • XA 54100  (3)
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  • Medicine  (3)
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  • 1
    Online Resource
    Online Resource
    Brucella species release a specific, protease-sensitive, inhibitor of TNF-alpha expression, active on human macrophage-like cells.
    The American Association of Immunologists ; 1996
    In:  The Journal of Immunology Vol. 156, No. 8 ( 1996-04-15), p. 2885-2893
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 156, No. 8 ( 1996-04-15), p. 2885-2893
    Abstract: Brucella species can establish themselves and cause disease in humans, but the mechanisms by which brucellae evade the antibacterial defenses of their host remain largely unknown. We have previously reported that, unlike Escherichia coli K12, intracellular pathogens from the genus Brucella survive and multiply within U937-derived phagocytes, and live Brucella organisms failed to induce TNF-alpha release upon infection. Moreover, exogenously added TNF-alpha restricted intracellular growth of Brucella species. Herein, we demonstrate that Brucella-infected U937 cells are activated to express IL-1 beta and IL-6 at both the mRNA and protein levels, while they cannot accumulate TNF-alpha mRNA. When physically separated from macrophages, live brucellae impaired TNF-alpha production in E. coli-infected cells. Moreover, in agonist-activated macrophages, supernatants from Brucella cultures promoted an inhibition of the induction of both TNF-alpha expression and release, without affecting IL-1 beta or IL-6 induction. These phenomena, observed whatever the Brucella strain assayed, show that brucellae release some high m.w. factor(s) that specifically inhibits TNF-alpha expression in activated human macrophages. The proteic nature of the factor(s) was demonstrated by its heat and protease sensitiveness, and this could explain why U937-derived macrophages did release TNF-alpha when infected with chloramphenicol-treated brucellae. We also found that the Brucella factor(s) specifically acts on human macrophagic cells, but not on murine macrophage-like cells. Our findings provide direct evidence that a secreted Brucella virulence factor(s) inhibiting TNF-alpha expression might contribute to the evasion of Brucella organisms from human antimicrobial defenses.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.156.8.2885
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 1996
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
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    Online Resource
  • 2
    Online Resource
    Online Resource
    Differential effects of macrophage- and granulocyte-macrophage colony-stimulating factors on cytokine gene expression during rat alveolar macrophage differentiation into multinucleated giant cells (MGC): role for IL-6 in type 2 MGC formation.
    The American Association of Immunologists ; 1996
    In:  The Journal of Immunology Vol. 157, No. 11 ( 1996-12-01), p. 5118-5125
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 157, No. 11 ( 1996-12-01), p. 5118-5125
    Abstract: Macrophage colony-stimulating factor (M-CSF) and granulocyte-macrophage (GM)-CSF stimulate the differentiation of rat alveolar macrophages (AM) into multinucleated giant cells (MGC) with distinct phenotypes (type 1 and type 2 MGC). In the present study, we analyzed the profile of cytokine gene expression induced respectively, by M-CSF and GM-CSF during rat AM differentiation using reverse transcription-PCR. Enhanced mRNA expression for IL-1alpha, TNF-alpha, and TGF-beta1 was observed 3 h after treatment with M-CSF (50 U/ml) or GM-CSF (50 U/ml). In contrast, IL-6 mRNA expression was increased by GM-CSF but not M-CSF. Kinetic analysis indicated that GM-CSF stimulated IL-6 expression early (1.5 h), with maximal effect observed at 24 h and up to 5 days thereafter. Increased mRNA levels for IL-6 were associated with higher IL-6 activity in the culture media of differentiating AM. IL-6 activity was stimulated 3 h after treatment with GM-CSF and increased with time (up to 5 days). Interestingly, addition of exogenous IL-6 (20-100 ng/ml) alone or in combination with GM-CSF to AM cultures increased slightly and selectively the formation of MGC with type 2 phenotype. Conversely, neutralization of endogenous IL-6 during AM differentiation into MGC inhibited significantly (up to 50%) the formation of type 2 MGC. These results suggest a role for IL-6 in the formation of type 2 MGC and provide some insights into the mechanisms of MGC formation and the processes that regulate it positively.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.157.11.5118
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 1996
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
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    Online Resource
  • 3
    Online Resource
    Online Resource
    IL-1 stimulates a diverging signaling pathway in EL4 6.1 thymoma cells. IL-2 release, but not IL-2 receptor expression, is sensitive to pertussis toxin.
    The American Association of Immunologists ; 1995
    In:  The Journal of Immunology Vol. 155, No. 1 ( 1995-07-01), p. 181-189
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 155, No. 1 ( 1995-07-01), p. 181-189
    Abstract: We reassessed the involvement of Bordetella pertussis toxin (PTX)-sensitive proteins in the IL-1 signaling pathway on the responses induced by IL-1 on the murine thymoma cell line EL4 6.1. We demonstrate that the ADP-ribosyltransferase activity of PTX, and not its cell-anchoring B oligomer part, is responsible for the inhibition of IL-1-induced IL-2 release, since 1) the concentration of PTX ( & lt; or = 1 ng/ml) required to block the secretion is 100 to 1000 times lower than the concentration needed with the B oligomer; and 2) the mutated PT-9K/129G, devoid of ADP-ribosyltransferase activity, was inactive at 100 ng/ml. We found that partial ADP-ribosylation of the Gi2/Gi3 proteins before stimulation with IL-1 was sufficient to obtain full inhibition of IL-2 release. PTX did not however inhibit the appearance on the cell surface of the high affinity IL-2 receptors or the IL-2 release induced by PMA. In addition, we show that PTX prevented the expression of the IL-2 mRNA induced by IL-1, without affecting the binding of IL-2 specific nuclear factors to the T cell distal element of the IL-2 promoter. Furthermore, PTX also inhibited IL-1-induced proliferation of non-transformed thymocytes. In conclusion, our results demonstrate that IL-1-induced IL-2 release is sensitive to PTX-catalyzed ADP-ribosylation and that IL-1 activates a diverging pathway on EL4 6.1 cells.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.155.1.181
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 1995
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
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    Online Resource
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