title: Exposure to bisphenol A enhanced lung eosinophilia in adult male mice.
abstract: BACKGROUND
  Bisphenol A (BPA) is useful in many manufacturing processes and is also found in commonly used consumer products. Previous experimental studies have reported that perinatal exposure to BPA promotes the development of allergic lung inflammation in childhood and even into adulthood. In this study, the effects of BPA on allergic lung inflammation in adults were investigated in murine lungs.
  
  
  METHODS
  CD-1 mice were orally administrated with 1 mg of BPA/mouse four times at one-week intervals with or without ovalbumin (OVA). The pathologic changes in the airways, cytological alterations in bronchoalveolar lavage fluid (BALF), levels of inflammatory cytokines/chemokines in BALF, and OVA-specific IgE and IgG1 antibodies in serum were measured in the treated CD-1 mice. In vitro study using RAW264.7 cells, which are macrophage-like cells derived from BALB/c male mice, was conducted. The gene expression of cytokines and chemokines were measured.
  
  
  RESULTS
  BPA enhanced eosinophil recruitment induced by OVA in the alveoli and in the submucosa of the airway, which has a goblet cell proliferation in the bronchial epithelium. BPA increased Th2 cytokines-interleukin-13 (IL-13), eosinophil-relevant cytokines and chemokines, such as IL-5, and CCL2 induced by OVA, in BALF. BPA induced adjuvant effects on OVA-specific IgG1 production. In the in vitro study using RAW264.7 cells, BPA increased the mRNA expression of IL-1β, IL-6, CCL2 and CCL3 compared with the control and OVA groups.
  
  
  CONCLUSIONS
  These results suggest that (1) the exposure of BPA could synergize with an OVA challenge to aggravate the severity of lung eosinophilia in adult mice, possibly by promoting a Th2-biased immune response and (2) the activation of macrophages and inflammatory cytokines released from these cells by BPA could be participating in this phenomenon.
authors.affiliation: Environment and Non-communicable Disease Research Center, School of Public Health, China Medical University, Shenyang, 110122 China.
authors.forename: Miao
authors.initials: M
authors.lastname: He
authors.affiliation: Department of Health Sciences, Oita University of Nursing and Health Sciences, Oita, 870-1201 Japan.
authors.forename: Takamichi
authors.initials: T
authors.lastname: Ichinose
authors.affiliation: Department of Health Sciences, Oita University of Nursing and Health Sciences, Oita, 870-1201 Japan.
authors.forename: Seiichi
authors.initials: S
authors.lastname: Yoshida
authors.affiliation: Environmental Health Division, Department of Environmental Engineering, Graduate School of Engineering, Kyoto University, Kyoto, 615-8530 Japan.
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Takano
authors.affiliation: Environmental Chemistry Division, National Institute for Environmental Studies, Ibaraki, 305-8506 Japan.
authors.forename: Masataka
authors.initials: M
authors.lastname: Nishikawa
authors.affiliation: Department of Environmental Toxicology, University of California, Davis, CA 95616 USA.
authors.forename: Takayuki
authors.initials: T
authors.lastname: Shibamoto
authors.affiliation: Environment and Non-communicable Disease Research Center, School of Public Health, China Medical University, Shenyang, 110122 China.
authors.forename: Guifan
authors.initials: G
authors.lastname: Sun
keywords: Bisphenol A; Lung eosinophilia; Macrophage; Mice