title: Prenatal exposure to bisphenol A up-regulates immune responses, including T helper 1 and T helper 2 responses, in mice.
abstract: The effect of prenatal exposure to bisphenol A (BPA) on the immune system in mice was investigated. Virgin female mice were fed varying doses of BPA, on a daily basis, over a period of 18 days commencing on the day of pairing with stud males (day 0). On day 77, their male offspring of 8 weeks were immunized with hen egg lysozyme (HEL). Three weeks later, anti-HEL immunoglobulin G (IgG) in sera, and proliferative responses of spleen cells to the antigen, were measured. Anti-HEL IgG2a and interferon-gamma (IFN-gamma), secreted from splenic lymphocytes, were measured as indicators of T helper 1 (Th1) immune responses, while anti-HEL IgG1 and interleukin-4 (IL-4) were measured as indicators of Th2 responses. The results showed that fetal exposure to BPA was followed by significant increases in anti-HEL IgG as well as antigen-specific cell proliferation. Both Th1 responses (including anti-HEL IgG2a and IFN-gamma production) and Th2 responses (including anti-HEL IgG1 and IL-4 production) were augmented by prenatal exposure to BPA, although the augmentation of Th1 responses appeared to be greater than that of Th2 responses. Two-colour flow cytometric analysis showed that mice exposed prenatally to BPA had 29% and 100% more splenic CD3(+) CD4(+) and CD3(+) CD8(+) cells, respectively, than control animals. Similar results were obtained from females whose mothers had consumed BPA during pregnancy. These results suggest that prenatal exposure to BPA may result in the up-regulation of immune responses, especially Th1 responses, in adulthood.
authors.affiliation: Department of Pharmacology, Kobe Pharmaceutical University, Kobe, Japan. yoshino@kobepharma-u.ac.jp
authors.forename: Shin
authors.initials: S
authors.lastname: Yoshino
authors.forename: Kouya
authors.initials: K
authors.lastname: Yamaki
authors.forename: Xiaojuan
authors.initials: X
authors.lastname: Li
authors.forename: Tao
authors.initials: T
authors.lastname: Sai
authors.forename: Rie
authors.initials: R
authors.lastname: Yanagisawa
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Takano
authors.forename: Shinji
authors.initials: S
authors.lastname: Taneda
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Hayashi
authors.forename: Yoki
authors.initials: Y
authors.lastname: Mori
mesh_terms: D000818:Animals; D001559:Benzhydryl Compounds; D017252:CD3 Complex / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D002455:Cell Division / Q000187:drug effects; D016207:Cytokines / Q000276:immunology; D004968:Estrogens, Non-Steroidal / Q000494:pharmacology*; D005260:Female; D007074:Immunoglobulin G / Q000276:immunology; D007371:Interferon-gamma / Q000276:immunology; D015847:Interleukin-4 / Q000276:immunology; D018655:Lymphocyte Count; D008297:Male; D051379:Mice; D010636:Phenols / Q000494:pharmacology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D013268:Stimulation, Chemical; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*; D014874:Water Pollutants, Chemical / Q000494:pharmacology*; D000098826:Bisphenol A Compounds
chemical_list: D001559:Benzhydryl Compounds; D017252:CD3 Complex; D016207:Cytokines; D004968:Estrogens, Non-Steroidal; D007074:Immunoglobulin G; D007371:Interferon-gamma; D015847:Interleukin-4; D010636:Phenols; D014874:Water Pollutants, Chemical; C006780:bisphenol A; D000098826:Bisphenol A Compounds