The study shows that both natural hormones like estrogen and man‑made chemicals that act like estrogen (such as BPA, certain plant compounds, and some livestock drugs) can lower the amount of thymosin‑alpha‑1 that thymus cells make, likely by binding to estrogen receptors on those cells. This was seen in mouse cells in a lab dish, so it hints that high estrogenic exposure might blunt your body’s own production of this immune‑boosting peptide.

The present study was carried out to assess the direct effect of natural estrogen and environmental estrogens on thymus epithelial cell (TEC) production/secretion of the thymic hormone thymosin-alpha 1 by using the technique of quantitative high-performance liquid chromatography. The presence of estrogen receptors in the TECs was also investigated. Murine TECs were cultured in the experimental DMEM medium containing various concentrations of natural or environmental estrogens, which was followed by determining the production of thymosin-alpha 1. The production of thymosin-alpha 1 by TECs was significantly inhibited by increasing concentrations of 17beta-estradiol (natural estrogen) over 3 x 10(-11) M, genistein (phytoestrogen) over 3 x 10(-9) M, coumestrol (phytoestrogen) over 3 x 10(-9) M, alpha-zearalanol (livestock anabolic) over 3 x 10(-7) and bisphenol-A (plastic) over 3 x 10(-6) M. Small amounts of estrogen receptor were present in the TECs. The above results clearly indicate that natural and environmental estrogens directly modulate TECs to produce thymic hormone probably through an estrogen receptor mechanism. Furthermore, our finding may be useful for evaluating biological effects of chemicals with estrogenic activity.