Abstract

Bisphenol A (BPA) is a common environmental endocrine disruptor which mimic the effect of estrogen. The immunotoxicity of BPA has attracted widespread attention in recent years. However, the effects and mechanism of BPA on autoimmune disease were rarely reported. Systemic lupus erythematosus (SLE) is a typical autoimmune disease, and its etiology and mechanism are complex and unclear. Currently, inflammation and the production of autoantibodies are considered to be important pathological mechanisms of SLE, and estrogen contributes to the occurrence and development of SLE. Therefore, in order to explore whether BPA exposure can affect the development of SLE and its possible mechanism, we used MRL/lpr (lupus-prone mice) and C57/BL6 female mice exposed to 0.1 and 0.2 µg/mL BPA for 6 weeks. We discovered that BPA exposure increased the concentration of serum anti-dsDNA antibody and IL-17, and the level of RORγt protein (the transcription factor of Th17 cells). Moreover, there were higher expression of p-PI3K, p-AKT, p-mTOR, ULK, Rubicon, P62, Becline1 and LC3 protein in spleen tissue of BPA exposed MRL/lpr mice compared with the control. However, there were no significant changes in the expression of IL-17, RORγt or mTOR in C57 mice exposed to BPA at the same dose. Our study implied that BPA exposure induced the development of SLE, which might be related to the up-regulation of PI3K/AKT/mTOR signaling pathway and abnormal autophagy. Our study indicated that lupus mice were more susceptible to BPA, and provided a new insight into the mechanism by which BPA exacerbated SLE. Therefore, our study suggested that autoimmune patients and susceptible population should be considered when setting thresholds for environmental BPA exposure.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.