Parental exposure to bisphenol A and its analogs influences zebrafish offspring immunity

Highlights: • Bisphenol A and its analogs bioaccumulated in zebrafish offspring via the transfer of parental waterborne bisphenols burdens. • Parental exposure to bisphenol A and its analogs decreased survive of zebrafish offspring. • Parental exposure to bisphenol A and its analogs influenced zebrafish offspring immunity. • Parental exposure to bisphenol A and its analogs could result in a decreased healthy status in zebrafish offspring. Transgenerational effects of environmental pollutants on humans and animals are complex. Thus, we used zebrafish to evaluate the effects of parental whole-life cycle exposure to bisphenol A and its analogs (bisphenol S and F) on offspring innate immunity. At adulthood, offspring were examined with/without continued chemicals treatment until 72 h post-fertilization (hpf). To measure offspring immune function, larvae at 72 hpf were expose for 24 h with/without the viral mimic polyinosinic-cytidylic acid (Poly I:C) or the bacterial mimic Pam3Cys-Ser-Lys4 (PAM3CSK4). Data show modified immunity in offspring. Specifically, lysozyme activity was significantly induced in F1 larvae and respiratory burst response and oxidative defense genes were inhibited. Genes of the innate immune system including Toll-like receptors and their downstream molecules and inflammatory cytokines were significantly down-regulated, whereas matrix metalloproteinases were up-regulated in larvae. In addition, recombination-activating genes in the immature adaptive immune system were significantly reduced. Thus, immune defense is diminished by exposing parental generations of zebrafish to environmentally relevant concentration of bisphenols and this suggests that fish chronically exposed to bisphenols in the wild may be vulnerable to pathogens.