Bisphenol A Activates an Innate Viral Immune Response Pathway

Bisphenol A (BPA) is a ubiquitous component in the manufacturing
of plastic. It is commonly found in food and beverage containers.
Because of its broad exposure and evidence that it may act as an estrogen-like
molecule, many have studied its potential effects. For example, epidemiological
studies have found an association between in utero BPA exposure and
onset of childhood asthma. Our previous work suggested BPA treated
mice induced asthma-like symptoms in both mothers and their pups.
In order to better understand theconsequences of BPA exposure and
potential mechanisms, we used a proteomics approach. Using both CD4+ T cells from an in vivo model of BPA exposure and an in vitro
epithelial cell model, we identified activation of both innate and
adaptive immune signaling following BPA exposure. Furthermore,
our proteomic results from our multigenerational mouse model study
implicates aberrant immune activation across several generations.
We propose the following; BPA can active an innate viral immune response
by upregulating a probable palmitoyltransferase ZDHHC1, and its
binding partner stimulator of interferon-gamma (STING). It also has
additional histone epigenetic perturbations, suggesting a role for
epigenetic inheritance of these immune perturbations.