Open AccessBisphenol A in combination with TNF-α selectively induces Th2 cell-promoting dendritic cells in vitro with an estrogen-like activity
Author(s) -
Hongchuan Guo,
Tianyi Liu,
Yukari Uemura,
Shunchang Jiao,
Deqing Wang,
Zilin Lin,
Yayoi Narita,
Motoharu Suzuki,
Narumi Hirosawa,
Yasuko Ichihara,
Osamu Ishihara,
Hirosato Kikuchi,
Yasushi Sakamoto,
Satoru Senju,
Qiuhang Zhang,
Feng Ling
Publication year - 2010
Publication title -
cellular and molecular immunology/cellular and molecular immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.5
H-Index - 81
eISSN - 2042-0226
pISSN - 1672-7681
DOI - 10.1038/cmi.2010.14
Subject(s) - tumor necrosis factor alpha , bisphenol a , chemistry , immune system , in vitro , chemokine , endocrinology , immunology , medicine , biochemistry , organic chemistry , epoxy
Bisphenol A (BPA) is a monomer used in manufacturing a wide range of chemical products, including epoxy resins and polycarbonate. BPA, an important endocrine disrupting chemical that exerts estrogen-like activities, is detectable at nanomolar levels in human serum worldwide. The pregnancy associated doses of 17beta-estradiol (E2) plus tumor-necrosis factor-alpha (TNF-alpha) induce distorted maturation of human dendritic cells (DCs) that result in an increased capacity to induce T helper (Th) 2 responses. The current study demonstrated that the presence of BPA during DC maturation influences the function of human DCs, thereby polarizing the subsequent Th response. In the presence of TNF-alpha, BPA treatment enhanced the expression of CC chemokine ligand 1 (CCL1) in DCs. In addition, DCs exposed to BPA/TNF-alpha produced higher levels of IL-10 relative to those of IL-12p70 on CD40 ligation, and preferentially induced Th2 deviation. BPA exerts the same effect with E2 at the same dose (0.01-0.1 microM) with regard to DC-mediated Th2 polarization. These findings imply that DCs exposed to BPA will provide one of the initial signals driving the development and perpetuation of Th2-dominated immune response in allergic reactions.