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Long‐term exposure to high levels of decabrominated diphenyl ether inhibits CD4 T‐cell functions in C57Bl/6 mice
Author(s) -
Feng Yan,
Zeng Weihong,
Wang Ying,
Shen Hao,
Wang Yan
Publication year - 2016
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.3270
Subject(s) - immunology , immune system , population , cytokine , antigen , chemistry , biology , medicine , environmental health
In recent years, the adverse health effects of decabrominated diphenyl ether (BDE‐209) have raised more concerns as a growing number of studies reported its persistence in the environment and abundance in the human population, especially in occupational environmental compartments and exposed personnel. This study applies our previous animal model simulating occupational exposure to BDE‐209 to investigate its potential adverse effects on CD4 T cells. Female C57Bl/6 mice were orally gavaged with BDE‐209 at a dose of 800 mg kg −1 every 2 days for 10 months and the blood of each mouse was collected for analysis. Kinetic changes of the peripheral immune system were investigated from 1 to 5 months of exposure. The chronic effects on cytokine production, proliferation and the antigen‐specific responses of CD4 T cells were evaluated at 7, 9 and 10 months, respectively. The results have shown that impaired proliferation and cytokine (IFN‐γ, IL‐2 or TNF‐α) production of CD4 T cells were observed in BDE‐209‐exposed mice, accompanied by increased T regulatory cells in the blood. BDE‐209 exposure in vitro also suppressed the reactivity of CD4 T cells at concentrations of 0.01, 0.1, 1 and 10 μM. Furthermore, we observed weaker antigen‐specific CD4 T‐cell responses to Listeria monocytogenes infection in the mice exposed to BDE‐209, suggesting decreased resistance to exogenous pathogens. Taken together, these observations indicate an impaired cellular immunity after long‐term and relative high‐dose exposure to BDE‐209 in adult mice. Copyright © 2015 John Wiley & Sons, Ltd.

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