Expresion Of IL-1βin Hydatidiform Mole Patients Without NLRP7Mutation

Backgroud:Hydatidiform mole is a most common abnormal conception of excessive trophoblast development resulting in abnormal human pregnancies with no embryo and cystic degeneration of the chorionic villi. Although it is a benign disease and the pathological changes are often restricted to the uterine cavity, it trends to recurring. It occurs in1in every1500pregnancies in western societies and Europe. It is2-10times higher in some countries of Latin America, the Middle East, and the Far East with the highest frequencies being in Mexico, Iran, and Indonesia. The results of hydatidiform mole are usually unsatisfactory, especially the recurrent hydatidiform mole. However, with regarding to the pathogenesis of hydatidiform mole, it has not been understood thoroughly, though the researchers at home and abroad have done lots of researches on it. It is said the pathogenesis of hydatidiform mole has something to do with the gene mutation, growing age, environment and disfunctions of immunology.Recently, researchers have displayed that the growth of hydatidiform mole tissues in uterine cavity was associated with the abnormal expression level of immune cells, such as B cell, T cell, and histocytes. In2006, with the help of the gene cloning positioning, researches found that the mutations of NLRP7gene have something to do with the family recurrent hydatidiform mole and Women with recurrent HMs are homozygous or compound heterozygous for mutations in NALP7. In China,48%of Chinese patients with at least2hydatidiform moles have NLRP7mutations, while the rate in Pakistani and Indian patients is81and84%, respectively. Overexpression of NLRP7in vitro inhibits IL-1β production upon stimulation with lipopolysaccharide (LPS), a component of the cell walls of gram-negative bacteria known to cause fetal loss in human and animals. However, among a large number of sporadic and non family inherited hydatidiform mole patients, there was no NALP7gene mutations. Then, is there any abnormal secretion in the non family inherited hydatidiform mole patients? Through the research on the above questions, it will be very useful to understand the pathogenesis of hydatidiform mole thoroughly and find other genes to explain the mechanism of hydatidiform mole.In the present study, we detected the expression and relationship between IL-1(3and Hydatidiform mole patients without NLRP7mutations, using the method of enzyme-linked immunosorbent assay.Objective:To detect the expression and relationship between IL-1β and Hydatidiform mole patients without NLRP7mutations.Methods:Compare the expression of IL-1β in the leukomonocytes derived from Peripheral Blood (PB) of women with normal and Hydatidiform mole pregnancy without NLRP7 mutations after adding LPS, using enzyme-linked immunosorbent assay (ELISA).Results:In comparison to women with normal and Hydatidiform mole pregnancy, there was no significant difference in the expression level of IL-1βp (P=0.532) before aiding LPS. The expression level of IL-1β in hydatidiform mole and normal person was0.879,0.987, respectively. After adding LPS, the expression level in each group increased to0.934,1.151, respectively. The expression in normal group was significant higher than hydatidiform mole group (P=0.008). In the women with normal pregnancy group, the expression level of IL-1β after adding LPS was much higher than that without adding LPS (P=0.008). However, in the women with Hydatidiform mole pregnancy, there was not significant different (P=0.074).Conclusion:IL-1β might exert distinct regulatory actions on the pathogenesis of human Hydatidiform mole. This role might be achieved through the autoimmunity disfunction of the women of Hydatidiform mole pregnancy.