These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Differential inhibitory effects of interleukin-10, interleukin-4, and dexamethasone on staphylococcal enterotoxin-induced cytokine production and T cell activation.
    Author: Krakauer T.
    Journal: J Leukoc Biol; 1995 Mar; 57(3):450-4. PubMed ID: 7884317.
    Abstract:
    The cytokine profile of human peripheral blood mononuclear cells (PBMC) stimulated by staphylococcal enterotoxin (SE) A and B was examined. Production of tumor necrosis factor (TNF alpha), interleukin (IL)-1, IL-6, IL-2, and gamma interferon (IFN-gamma) was observed. In contrast, Th2 cytokines IL-4 and IL-10 were absent from SEA- or SEB-stimulated PBMC. Moreover, adding IL-10 to SE-stimulated PBMC inhibited the production of IL-1, IL-6, TNF alpha, and IFN gamma by 50 to 80% but had less effect (8-30%) on T cell proliferation. IL-4 was less effective than IL-10 in inhibiting cytokine production and enhanced T cell proliferation by SEA or SEB. The anti-inflammatory agent, dexamethasone, was the most potent agent in controlling the SE-mediated effects as evidenced by inhibited T cell proliferation (55%) and reduced levels of IL-1, IL-6, and IFN gamma (60% to 100%) and TNF alpha (50%). Reducing levels of toxic mediators such as TNF alpha, IL-1, IL-6, and IFN gamma by dexamethasone in SE-induced T cell responses may be a useful therapeutic strategy to circumvent SE toxicity and pathogenesis.
    [Abstract] [Full Text] [Related] [New Search]