Exposure to Bisphenol A Prenatally or in Adulthood Promotes TH2 Cytokine Production Ass... - 0 views
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BPA promotes the development of TH2 cells in adulthood and both TH1 and TH2 cells in prenatal stages by reducing the number of regulatory T cells.
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Prenatal exposure to BPA has been shown to alter a variety of reproductive endocrine parameters, such as testosterone and luteinizing hormone levels
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Exposure to BPA by subcutaneous injection in adulthood significantly promoted antigen-stimulated production of IL-4, IL-10, and IL-13 in TH2-skewed
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We showed that prenatal exposure to BPA increased the production of a TH1 cytokine, IFN-γ, and a TH2 cytokine, IL-4, after the offspring developed, suggesting that prenatal exposure to BPA can induce persistent immunologic effects lasting into adulthood.
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These results are consistent with a previous report that fetal exposure to BPA augmented TH1 and TH2 immune responses
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our results clearly demonstrate that the production of TH2 cytokines is promoted by BPA in adult mice and in offspring during developmental exposure.
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The decrease of Treg cells would predispose to immune dysfunction in aged individuals, explaining their higher risk of immune-mediated diseases, cancer, and infections.
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BPA might cause these diseases. Thus, avoiding exposure to or promoting the excretion of BPA and other EDCs would help in preventing diseases and adverse health effects.