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Effects of bisphenol A on antigen‐specific antibody production, proliferative responses of lymphoid cells, and TH1 and TH2 immune responses in mice
Author(s) -
Yoshino Shin,
Yamaki Kouya,
Yanagisawa Rie,
Takano Hirohisa,
Hayashi Hideyuki,
Mori Yoki
Publication year - 2003
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0705166
Subject(s) - immune system , antigen , antibody , spleen , biology , endocrinology , immunology , medicine , secretion
We investigated the effect of bisphenol A (BPA), which binds estrogen receptors, on immune responses including production of antigen‐specific antibodies, proliferative responses of lymphoid cells, and Th1 and Th2 responses. For this investigation, mice were p.o. given varying doses including 3, 30, 300, and 3000 μ g kg −1 of BPA immediately after immunization with hen egg lysozyme (HEL) (day 0) and then daily by day 20. On day 21, anti‐HEL IgG antibodies in sera and proliferative responses of spleen cells to the antigen were measured. Anti‐HEL IgG2a antibodies and IFN‐ γ secreted from splenic lymphocytes were also measured as indicators of Th1 immune responses, while anti‐HEL IgG1 antibodies and IL‐4, as those of Th2 responses. The results showed that treatment with 3000 μ g kg −1 of BPA was followed by a significant increase in anti‐HEL IgG as well as the antigen‐specific cell proliferation. Anti‐HEL IgG2a production and IFN‐ γ secretion were significantly enhanced in mice treated with 300 and 30 μ g kg −1 of BPA, respectively, while anti‐HEL IgG1 production and IL‐4 secretion were augmented in animals given 3000 and 300 μ g kg −1 of the chemical, respectively. Augmentation of these immune responses was also observed in mice exposed to 0.3–30 μ g kg −1 of estradiol, although Th1 responses appeared to be more sensitive to the sex hormone than Th2 responses. These results suggest that BPA may play a role in augmenting immune responses, especially Th1 responses.British Journal of Pharmacology (2003) 138 , 1271–1276. doi: 10.1038/sj.bjp.0705166

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