Journal of Reproductive Immunology最新文献

Male infertility has become a worldwide concern. Millions of couples today struggle with reproductive problems that result in infertility. While in many cases the underlying cause is unknown, in some cases the problem is with the man. The gradual increase in male fertility problems in recent decades suggests that factors beyond genetics or lifestyle may be involved. In recent years, exposure to environmental pollutants, including endocrine-disrupting chemicals, has attracted the attention of many researchers. One such substance is bisphenol A, which has been the subject of a flood of research due to its widespread use in everyday materials such as plastics, food containers, and thermal paper. This substance is capable of affecting the endocrine system by interfering with hormonal systems. Although bisphenol A has been discussed as a disruptor until now, emerging evidence suggests that its impact is much greater. The testes have a unique immune setting, known as the testicular immune microenvironment (TIM), which maintains a balance between immune tolerance and the protection of germ cells. Studies suggest that BPA can disturb this balance by altering macrophage behavior, changing cytokine patterns, activating mast cells, and affecting T cell function. These immune changes can weaken testicular immune privilege and disturb sperm development. This review looks at BPA as a local immune disruptor in the male reproductive tract, linking hormonal effects with immune imbalance. Understanding BPA from this angle may help explain unexplored aspects of male infertility and guide future prevention effort.

Spontaneous preterm birth (SPTB) includes two distinct presentations: preterm labor with intact membranes (PTL-IM) and preterm premature rupture of membranes (PPROM), both associated with inflammation. In prior work, we identified first-trimester serum CX3CL1, a membrane-bound chemokine cleaved by the metalloprotease ADAM10, as an independent predictive blood biomarker for PPROM. The present study aimed to characterize the expression of ADAM10 and CX3CL1 in fetal membranes and maternal serum across gestation, and to assess serum ADAM10 as a potential predictive biomarker for SPTB. mRNA and protein expression of CX3CL1 and ADAM10 was assessed in 26 fetal membranes (amnion and choriodecidua). Serum ADAM10 was measured in a prospective cohort of 438 pregnant women with samples collected in the first trimester, second trimester and delivery. CX3CL1 expression increased in the choriodecidua during the second trimester and declined at term. ADAM10 mRNA remained stable in the amnion, while protein levels peaked in the choriodecidua in the second trimester and at term. Serum ADAM10 showed a similar pattern, with significantly higher levels in second-trimester PTL-IM cases versus term deliveries. Second trimester serum ADAM10 significantly enhanced the predictive ability of maternal risk factors for PTL-IM. Area under the ROC curve was 0.73 (95 % confidence interval: 0.65-0.81). This model identified cases with a 72 % (59 %-82 %) sensitivity and a 64 % (55 %-72 %) specificity. ADAM10 and CX3CL1 are expressed in the fetal-maternal interface, and their soluble forms measured in blood may help in the early identification of SPTB.

Toll-like receptors (TLRs) and NOD-like receptors (NLRs) are crucial pattern recognition receptors that initiate inflammatory responses and immunological activation upon detecting pathogen- or damage-associated molecular patterns (PAMPs/DAMPS) in the female reproductive tract, thereby maintaining homeostasis and supporting pregnancy success. Their signaling pathways play a significant role in reproductive disorders by mediating the immune response to various pathogenic stimuli. Recurrent pregnancy loss (RPL), defined as the natural ending of two or more pregnancies before 24 weeks of gestation, approximately half of these patients remain idiopathic without precise prognostic, diagnostic, and therapeutic plans. Emerging data point that microRNAs are essential for immunological control in the female reproductive tract. MicroRNAs (miRNAs) are non-coding RNAs that regulate gene expression by binding to mRNA and preventing translation into protein. miRNAs play a role in many biological processes, including the development and differentiation of trophoblasts, the activation and implantation of embryos, immune tolerance, and the receptivity of the endometrium during implantation. Given their capacity to regulate up to 30 % of the human genome, miRNAs offer a promising avenue for understanding the immunopathogenesis of pregnancy complications. Recent research has detected differential expression of specific miRNAs in reproductive system pathologies. This review focuses on microRNAs and their association with idiopathic recurrent miscarriage, a condition characterized by considerable heterogeneity. Future studies identifying the precise mechanisms linking miRNA-mediated immune dysregulation in RPL immunopathogenesis could open the way for novel personalized therapeutic and diagnostic strategies.

Endometriosis, a debilitating disease characterized by chronic inflammation, might be associated with adverse pregnancy outcomes. However, the long-term health implications for offspring born to mothers with endometriosis remain inadequately explored. The maternal immune response in pregnancy is crucial for fetal development and growth, and the pro-inflammatory state of endometriosis may alter fetal immunologic programming. We aimed to assess an association between fetal exposure to maternal endometriosis and long-term risk of infectious morbidity for the offspring. We conducted a retrospective population-based cohort study, comparing offspring of mothers with and without endometriosis. We followed the offspring longitudinally, tracking the time to their first diagnosis with an infectious disease made in a community-based clinic or hospitalization. A hazards plot was used to compare the cumulative incidence of offspring infectious morbidity between the study groups. A Cox regression model was constructed to evaluate an association between maternal endometriosis and offspring infectious morbidity, adjusting for possible confounders. A total of 232,476 singleton deliveries were included; 224 deliveries of mothers with endometriosis were compared to those without endometriosis. The cumulative incidence of infectious morbidity in offspring born to mothers with endometriosis was higher, using a hazards plot (p = 0.005). Likewise, a Cox regression model, adjusted for gestational age, fertility treatments, cesarean delivery, maternal diabetes, obesity, smoking and mother age at birth found that fetal exposure to maternal endometriosis was an independent risk factor for long-term infectious morbidity of the offspring (adjusted HR 1.17, 95 %CI 1.01-1.36, p = 0.049). In gestational age-stratified analyses, the association between maternal endometriosis and offspring infectious morbidity was driven primarily by term-born offspring. Fetal exposure to maternal endometriosis is an independent risk factor for long-term infectious morbidity of the offspring.