Study On The Effect Of Iodine Excess On The Induction Of EAT In Rats With Different Susceptibility

Autoimmune thyroid diseases (AITD) as the organ -specific autoimmune diseases are very common in human. Many factors such as individual genetic susceptibility, autoimmunity, endocrinology and environmental conditions are involved in the initiation and development of AITD. In recent years, it shows that there are differences in susceptibility to experimental autoimmune thyroiditis (EAT) between the animals of different strain. So it suggests that individual genetic susceptibility plays the important role in the development of AITD. In addition, epidemiological retrospect study and animal study have approved that there are obvious relations between iodine and incidence of AITD and production of thyroid autoantibodies. Iodine as another important factor affects the pathogenesis of AITD. Therefore, we study the pathogenesis of AITD from iodine and susceptibility. 1. The effect of iodine on the induction of EAT in rats with different susceptibilityStudy the effect of iodine and susceptibility on the pathogenesis of autoimmune thyroiditis. Establish the EAT model in susceptible and unsusceptible rats with the different iodine intake levels by immunization with thyroglobulin of porcine. Observe the pathological changes and infiltration of lymphocyte in thyroid tissue of rats. Detect the serum TGAb, TPOAb, T₃ and T₄ by the method of radioimmuoassay (RIA). Results:(1) The thyroids of Lewis and Wistar rats with EAT were infiltrated by lymphocyte and the more intake of iodine, the more serious the inflammation is. At the same level of iodine intake, the inflammation of Lewis rats with EAT was more serious than that of Wistar rats with EAT.(2) At the same level of iodine intake, the serum TPO-Ab of Lewis rats with EAT was significantly higher than that of Wistar rats with EAT (P<0.01) . The concentration of TG-Ab and TPO-Ab became strong with the increase of iodine intake.(3) The level of T₄ was lower in the rats administered with 100 times iodine intake (P<0.05). There was no statistical significant difference in T₃ between the groups.Conclusions:(1) The reaction of inflammation in the susceptible Lewis rats with EAT was more serious thanthat in the unsusceptible Wistar rats with EAT. The serum TPO-Ab of Lewis rats with EAT wassignificantly higher than that of Wistar rats with EAT.(2) High iodine intake could obviously aggravate the inflammation reaction of thyroid glands of rats with EAT and facilitate the development of EAT. The role of high iodine intake was more significant in the susceptible rats.(3) The inflammation reaction of thyroid of rat with EAT was consistent with the level of serum TPO-Ab. The relationship between TPO-Ab and development and pathological changes of EAT was much closer.(4) There are no statistical significance between Lewis rats with EAT and Wistar rats with EAT in serum levels of TG-Ab. But serum level of TPO-Ab in Lewis rats with EAT is significantly higher than that of Wistar rats with EAT. Therefore, it suggests that Iodine excess plays the different role in the induction of EAT in rats with different susceptibility.