Perinatal bisphenol A exposures increase production of pro-inflammatory mediators in bone marrow-derived mast cells of adult mice

摘要: Bisphenol A (BPA) is a widely used monomer of polycarbonate plastics and epoxide resin that has been implicated in asthma pathogenesis when exposure occurs to the developing fetus. However, few studies have examined relationship between perinatal BPA adulthood. This study an isogenic mouse model examine influence via maternal diet on inflammatory mediators associated with 6-month-old adult offspring by measuring bone marrow-derived mast cell (BMMC) production lipid (cysteinyl leukotrienes prostaglandin D2), cytokines (interleukin [IL]-4, IL-5, IL-6, IL-13, tumor necrosis factor [TNF]-α), histamine. Global DNA methylation levels BMMCs from were determined elucidate potential regulatory mechanism linking phenotype later life. Four doses tested: low (50 ng BPA/kg diet, n = 5), medium μg 4), high mg control (n 3). Following BMMC activation, increases cysteinyl leukotriene (p < 0.01) TNFα 0.05) observed all BPA-exposure groups, D2 IL-13 group. Additionally, mice groups displayed decrease global compared animals. Thus, long-term cell-mediated pro-inflammatory levels, suggesting for dysregulation, which could affect pulmonary inflammation allergic airway disease into