Environmental estrogen exposures alter molecular signaling in immune cells that promote the development of childhood asthma

Environmental estrogens (EEs) are associated with an increased prevalence of asthma. These epigenetic alterations of the immune cells may explain the multigenerational effects on asthma development. We hypothesized that exposure to immune cells enhances allergic sensitization by initiating signaling in these cells. Human T cell lines (TIB-152, CCL-119) were exposed to varying concentrations of estradiol, bisphenol A, bisphenol S, or bisphenol A + estradiol. H3K27me3, phosphorylations of EZH2 (pEZH2), AKT (pAKT), and phosphatidylinositide 3-kinase (pPI3K) were assessed. pAKT and pPI3K were decreased in response to some of the concentrations of these exposures in both cell lines. It is likely that EEs exposure to immune cells is one of the factors in the increase in the prevalence of asthma. •We observed the altered pAKT/pPI3K, pEZH2, and H3K27me3 in human T cells in response to endogenous and exogenous estrogens.•The pathway of rapid estrogen receptor signaling on these cells is likely different from reproductive cells.•It is likely that estrogen exposure to immune cells is one of the factors in the increase in the prevalence of asthma.