Aims: Autoimmune thyroiditis (AIT) is a common cause of thyroid disease, characterised by auto-antibodies targeting proteins of the thyroid gland. AIT impact 1 in 5 women and is strongly associated with infertility and reproductive complications. However, there is limited research looking into how thyroid antibodies lead to reproductive dysfunction. Our laboratory has established two models of AIT to investigate how fertility is impacted by the two major thyroid antibody types, thyroglobulin-antibodies (TGAb) and thyroperoxidase antibodies (TPOAb).
Methods: For our model of TGAb positivity, Lewis rats were provided sodium iodide in their drinking water (n=10 per group) and were injected with porcine thyroglobulin (2ng/ml) and Freund’s adjuvant. For our TPOab model, Sprague Dawley rats were provided standard drinking water and injected with recombinant TPO protein (0.6ug/ul) and Freund’s adjuvant. Control rats in each model received standard drinking water and were injected with vehicle controls. Estrous cycling was monitored using vaginal electrical impedance and cytology. Plasma was collected to assess thyroid antibody and hormone levels. Animals were mated and culled at embryonic day 20.
Results: Plasma TGAb was increased in AIT rats compared to controls and was associated with increased thyroxine without changes to TSH. TGAb impaired estrous cyclicity and fertility. Thyroglobulin-antibodies did not impact litter size but did cause reduced male fetus survival. Data collection from the TPO model is ongoing.
Conclusions: The findings from these models demonstrate that even a modest elevation in thyroid antibodies can lead to changes in fertility and reproductive health. These findings highlight the importance of using rodent models to investigate underlying pathophysiological causes impacting reproductive health.