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    Inhibition of superantigen-induced T cell proliferation and monocyte IL-1 beta, TNF-alpha, and IL-6 production by acute ethanol treatment

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    Authors
    Szabo, Gyongyi
    Mandrekar, Pranoti
    Catalano, Donna
    UMass Chan Affiliations
    Department of Medicine, Rheumatology Division
    Department of Surgery
    Department of Medicine, Division of Gastroenterology
    Document Type
    Journal Article
    Publication Date
    1995-09-01
    Keywords
    Adult
    Ethanol
    Female
    Gene Expression
    Humans
    Interleukin-1
    Interleukin-6
    Lymphocyte Activation
    Male
    Middle Aged
    Monocytes
    Superantigens
    T-Lymphocytes
    Tumor Necrosis Factor-alpha
    Life Sciences
    Medicine and Health Sciences
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    Link to Full Text
    https://doi.org/10.1002/jlb.58.3.342
    Abstract
    Alcohol use has been shown to decrease monocyte antigen presentation capacity and inflammatory cytokine production, thereby increasing susceptibility to infections. Here, we demonstrate that in vitro acute treatment of normal monocytes with pharmacological doses of ethanol can decrease superantigen [Staphylococcus enterotoxins B (SEB) and A (SEA)]-induced T cell proliferation. Furthermore, ethanol treatment (25-100 mM) significantly inhibited SEA- or SEB-induced production of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and IL-6 in monocytes. Ethanol-induced down-regulation of monocyte TNF-alpha, IL-1 beta, and IL-6 occurred at both the protein and mRNA levels. Additional data suggest that ethanol can decrease IL-1 beta mRNA stability. Furthermore, experiments using cycloheximide indicate that de novo protein synthesis is required for the inhibitory effect of ethanol on SEB-induced IL-1 beta mRNA production. Finally, ethanol treatment decreased HLA-DR expression in monocytes, suggesting that ethanol treatment can compromise monocyte stimulation by down-regulating the SEB-binding capacity of monocytes. These results suggest that acute ethanol treatment can interfere with monocyte activation by SEB at multiple steps. Consequently, decreased superantigen-induced polyclonal T cell activation and inflammatory monokine production would contribute to an impaired immune response to bacterial challenge with superantigens after acute alcohol intake.
    Source

    J Leukoc Biol. 1995 Sep;58(3):342-50.

    DOI
    10.1002/jlb.58.3.342
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/38273
    PubMed ID
    7665990
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    Link to Article in PubMed

    ae974a485f413a2113503eed53cd6c53
    10.1002/jlb.58.3.342
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