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Toxoplasma gondii (Toxoplasma gondii) is a zoonotic pathogen of toxoplasmosis, is one of the causative agents of human TORCH syndrome. Toxoplasma infection during pregnancy can be caused by vertical transmission of miscarriage, premature birth, birth defects and other adverse pregnancy outcomes, including early pregnancy Toxoplasma infection on pregnancy outcome in the most severely affected. Under normal circumstances, the maternal-fetal interface is a complex immune balance state. For the formation of the detailed mechanisms of this immune balance and immune molecules involved are not fully understood, but many studies have proven that the maternal-fetal interface MHC molecules and NK cells and their receptors play a crucial in the process of maintaining normal pregnancy role. It has been confirmed that HLA-G expression in human trophoblast cells and maternal decidual NK cell surface inhibitory receptor ligand to each other, and the combination of the two can effectively suppressing the maternal NK cells in the immune rejection of the embryo, in play an important role in maintaining normal pregnancy. Our previous studies have found that Toxoplasma infection can be lowered first trimester trophoblast layer cell surface HLA-G and human decidua NK cell inhibitory receptor expression (to be published). Therefore, this study intends to explore the above molecular mechanism of action of Toxoplasma gondii infection in adverse pregnancy outcomes in the body through the establishment of Toxoplasma gondii infection in animal models of early pregnancy. RT.BM1 RT1-E expression in the rat placenta the MHC Ib class of molecules, and the human HLA-E and HLA-G there are many similarities, suggesting RT.BM1 RT1-E may be adopted and expression in decidual corresponding NK cell surface receptors such as inhibitory receptors NKG2A and activating receptor NKG2C and Ly49s3 combined immune regulation of decidual NK cells activity, and thus play an important role in rats maintain normal pregnancy. So far, the rats with normal pregnancy process placental RT.BM1, RT1-E and decidual NK cell receptors NKG2A expression law NKG2C and Ly49s3, and Toxoplasma gondii infection adverse pregnancy outcomes both at home and abroad has not yet reported. This study on the basis of building a rat model of Toxoplasma gondii infection in early pregnancy, detect normal and infected group placenta RT.BM1 in rats, RT1-E and rat decidual NK cell receptors NKG2A, NKG2C, Ly49s3 mRNA expression level, the first to explore the expression pattern of the molecules in the course of a normal pregnancy, and then study the early pregnancy Toxoplasma infection the above molecule expression, analysis of their expression level changes and Toxoplasma infection in adverse pregnancy outcomes, and to explore the early pregnancy Toxoplasma gondii infection lead to adverse pregnancy outcomes molecular mechanism to add new content. 48 pregnant rats were randomly divided into the infected group and the normal group, n = 24. Infection group in the first five days of pregnancy intraperitoneal injection of 1 × 105 Toxoplasma gondii virulent strain (RH strain) tachyzoites / only the normal group without any treatment. 9,13,15,17 days pregnant two groups in six pregnant rats were sacrificed, sterile laparotomy observe fetal rat total recorded the stillbirth number of live births, number. The placenta RT.BM1, RT1-E and decidual NKG2A, NKG2C and Ly49s3 mRNA expression levels were detected. Results: (1) normal group, the number of live births to 204, stillbirth number three, the stillbirth rate was 1.4%; infection group, the number of live births to 133, stillbirth 27, the stillbirth rate was 16.9%, apparent the infection group stillbirth rate higher than the normal group, the difference was significant (P lt; 0.05). ② RT.BM1 mRNA: normal group 9,13,15 days expression levels are basically the same, and 17 days was significantly higher (P lt; 0.01); infection first three time points compared with the normal group was significantly higher (P lt ; 0.01). ③ RT1-E mRNA: normal group is lower than in the first nine days after the three time points (P lt; 0.05), while the infected group in 9,13,15 days were significantly increased as compared with the normal group, the difference was significant (P lt; 0.01), (P lt; 0.05), (P lt; 0.01). ④ NKG2A mRNA: 13 days expression levels were significantly higher than the other three time points (P lt; 0.05), the 9,15,17 days was no significant difference between; 9,13,15 days of the infected group were raised ( P lt; 0.05), (P lt; 0.01), (P lt; 0.01) in pregnant (days 13, 15) of the most significant. ⑤ NKG2C mRNA: 9,13 days highest expression was decreased 15, 17 days, a significant difference (P lt; 0.01) with the first two points in time; infected group at each time point were higher than the normal group, and 9 days, 13, 17-day infection group compared with the normal group, a significant difference (P lt; 0.01, P lt; 0.05, P lt; 0.05); ⑥ Ly49s3 mRNA: 13 days expression levels of the normal group was significantly higher than that of the other three times point (P lt; 0.01), the expression of the infected group at four time points were significantly increased (P lt; 0.01). The results of this study show the appropriate amount of Toxoplasma gondii infection animal model to establish successful; the above MHC molecules and NK cell receptor expression level is closely related with pregnancy progress; Toxoplasma infection during early pregnancy can cause the molecular expression level of change, breaking the normal pregnancy required the placenta local immune equilibrium may cause adverse pregnancy outcomes, one of the molecular mechanisms of Toxoplasma gondii infection in early pregnancy.
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