Abstract
Unexplained recurrent spontaneous abortion (URSA) is a common complication of pregnancy. Although tolerance of the maternal immune system is considered to be essential for a normal pregnancy, the precise mechanism underlying the pathogenesis of URSA remains to be fully elucidated, albeit it is known to involve inflammation. Here, we examine the relationship between the expression of inflammatory cytokines and the activation of downstream signaling pathways in URSA patients. Decidual and peripheral blood samples were collected from 30 URSA patients and from 30 women with normal early pregnancies. Western blot analysis was used to measure the expression levels of signal transducers and activators of transcription 3(STAT3), phosphorylated STAT3(p-STAT3), and interleukin-17 receptor(IL-17R) in the decidual samples. Enzyme-linked immunosorbent assay was used to assess the levels of IL-17, IL-10, IL-6, and IL-23 in the peripheral blood and decidual samples. In the URSA patients, the IL-10 expression levels were lower than those in the control subjects (P<0.05), whereas IL-6, IL-17, and IL-23 were all expressed at higher levels(P<0.05). Furthermore, the expression levels of IL-17R and p-STAT3 were higher in the URSA patients, exhibiting a trend similar to that of IL-23. Our finding of increased IL-23 expression in the deciduae and peripheral blood of patients with URSA suggest that this maybe a contributing factor to the pathogenesis of this disease. Likewise, STAT3 activation through its phosphorylation, which was associated with the IL-23 increase, may also be involved in URSA pathogenesis. However, the precise pathogenic mechanism requires further study.
Highlights
Recurrent miscarriage (RM), which occurs in 1%–5% of pregnancies [1], is defined as the occurrence of two or more pregnancy losses before the 20th week of gestation
The results of this study revealed that there is a similar trend of increased IL-23 and phosphorylated STAT3 (p-STAT3) expression in unexplained recurrent spontaneous abortion (URSA) patients, indicating that these molecules may contribute to the pathogenesis of URSA and may serve as potential therapeutic targets for its prevention
Increased p-STAT3 and IL-17R levels were detected in the decidual tissues of patients with URSA, compared with those in the control group (P< 0.05; Fig 3); there was no significant difference in the STAT3 expression levels between the two groups(P>0.05; Fig 3)
Summary
Recurrent miscarriage (RM), which occurs in 1%–5% of pregnancies [1], is defined as the occurrence of two or more pregnancy losses before the 20th week of gestation. In approximately 50% of cases, the precise cause remains unknown. Such cases, which occur primarily in the first trimester [2], are referred to as unexplained recurrent spontaneous abortion (URSA). Decidual tissue is essential for germ cell implantation and embryo development organization. It has the functions of nourishing the blastocysts, adjusting the endocrine milieu, regulating trophocyte invasion, and protecting the embryo from maternal rejection, playing an important role in normal pregnancy. Many studies have reported that the Th17/Treg paradigm plays a key role in the establishment and maintenance of maternal-fetal immune tolerance [6, 7]
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