Exposure to Bisphenol-A increases susceptibility to Trypanosoma cruzi infection.

Bisphenol-A (BPA), an endocrine disruptor, disrupts hormonal and chemical signaling within the body, negatively impacting health. One target of this disruption is the immune system. While BPA has been implicated in increased susceptibility to some pathogen infections, its effects on protozoan parasite infections remain understudied. This work evaluated the effect of BPA exposure on experimental Trypanosoma cruzi parasitemia in BALB/c mice. Parasitemia was evaluated in BALB/c mice by counting parasites in a Neubauer chamber. Additionally, ELISA assays were used to identify the presence of antibodies, cytokine gene expression was analyzed by RT-PCR, and liver marker levels were quantified using enzymatic kinetic methods. Both pre- and post-exposure to BPA increased parasitemia during T. cruzi infection and decreased levels of IgG1, IgG2a, and IgG2b isotypes. Furthermore, BPA modulated the expression of pro-inflammatory cytokines in response to infection. In addition, all mice exposed to BPA showed alterations in liver enzymes compared to the control group. These results demonstrate that the immune system during critical periods of T. cruzi infection is highly sensitive to BPA exposure, increasing susceptibility to the parasite.