Bisphenol A induces protection through modulation of the immune response against the helminth parasite Taenia crassiceps.

AIMS: Industrial growth has increased the exposure to endocrine disruptor compounds (EDCs) in all organisms. Bisphenol A (BPA), an EDC, has been demonstrated to be involved in the susceptibility to parasite infections. However, few studies have analysed this connection in more depth. The aim of this study was to determine whether early BPA exposure in female mice affects the systemic immune response and the susceptibility to Taenia crassiceps infection.

METHODS AND

RESULTS

BALB/c mice were exposed to BPA at post-natal day 3. At 6 weeks of age, they were inoculated with T crassiceps larvae and, 2 weeks later, were euthanized. The number of parasites was quantified. By flow cytometry, in the spleen, the peripheral and mesenteric lymph nodes, the different innate and adaptive immune cell modulation was analysed, and RT-PCR cytokine expression was also evaluated. BPA induced a reduction of 40% in parasite load. BPA treatment modulated some lineages of the innate immune response and caused slight changes in cells belonging to the adaptive immune response. Additionally, BPA enhanced the type 2 cytokine profile.

CONCLUSION

Neonatal BPA treatment in female mice affects not only the percentage of different immune cells but also their ex vivo cytokine gene expression, decreasing T crassiceps cysticercosis susceptibility.