Placenta最新文献_第5页

Increased protein O-GlcNAcYLATION in human placentas from hypertensive pregnancies 高血压妊娠人胎盘中o - glcnac酰化蛋白升高。

IF 2.5 2区医学 Q2 DEVELOPMENTAL BIOLOGY

Placenta

Pub Date : 2026-01-01 DOI: 10.1016/j.placenta.2025.05.024

Marta de Lima Castro , Rinaldo Rodrigues dos Passos Jr. , Thiago Lopes Rocha , Waldemar Naves do Amaral , Fernanda Regina Giachini

Introduction

Key proteins involved in placentation are susceptible to O-linked β-N-acetylglucosamine modification (O-GlcNAcylation). Anomalies in protein O-GlcNAcylation have been associated with pathological conditions, including hypertension, and it is known that arterial hypertension negatively impacts placental function. However, the precise impact of protein O-GlcNAcylation on placental function and fetal growth remains unclear in humans. Therefore, the current study aimed to investigate O-GlcNAcylation expression, and its catalytic enzyme O-GlcNAc transferase (OGT), in the placenta of pregnant women suffering from high blood pressure disorders.

Methods

Full-term placental samples were collected and divided into groups of normotensives (n = 11) or hypertensives women (n = 11). Western blotting and immunohistochemistry assessed O-GlcNAc and OGT expressions, and morphological characterization was conducted in all samples.

Results

In the hypertensive group, the maternal age (p = 0.041) was higher, whereas the gestational age (p = 0.004) and the newborn weight (p = 0.032) decreased, compared to the normotensive group. Morphometric analysis showed that the placentas from the hypertensive group displayed altered morphology, which was compatible with placentas from hypertensive mothers. Placental O-GlcNAc (p = 0.029) and OGT (p = 0.048) protein expression were higher in the hypertensive group. Augmented expression of O-GlcNAc was more predominant in the villi but also observed at the decidua.

Discussion

The present study demonstrates augmented protein O-GlcNAcylation and OGT expression in the placenta of pregnant with hypertensive disorders of pregnancy. In the future, the use of banks of placental tissue may be a useful strategy to map and identify candidates for O-GlcNAc modulation, requiring further evaluation.

引言：参与胎盘形成的关键蛋白易发生O-linked β- n -乙酰氨基葡萄糖修饰（o - glcnac酰化）。o - glcn酰化蛋白异常与包括高血压在内的病理状况有关，并且已知动脉高血压会对胎盘功能产生负面影响。然而，o - glcn酰化蛋白对人类胎盘功能和胎儿生长的确切影响尚不清楚。因此，本研究旨在探讨o - glcnac酰化及其催化酶O-GlcNAc转移酶（OGT）在高血压孕妇胎盘中的表达。方法：收集足月胎盘标本，分为血压正常组（n = 11）和高血压组（n = 11）。Western blotting和免疫组织化学检测O-GlcNAc和OGT的表达，并对所有样品进行形态学表征。结果：与正常组相比，高血压组产妇年龄增高（p = 0.041），胎龄增高（p = 0.004），新生儿体重下降（p = 0.032）。形态计量学分析显示，高血压组胎盘形态发生改变，与高血压母亲胎盘形态一致。高血压组胎盘O-GlcNAc （p = 0.029）和OGT （p = 0.048）蛋白表达较高。O-GlcNAc在绒毛中表达最多，在蜕膜中也有表达。讨论：本研究表明妊娠高血压疾病孕妇胎盘中o - glcn酰化蛋白和OGT表达增加。在未来，使用胎盘组织库可能是一种有用的策略来绘制和识别O-GlcNAc调节的候选物，需要进一步评估。

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引用次数: 0

Gestational diabetes mellitus affects the cross-talk among placental, maternal and umbilical cord vitamin D metabolites but fetal transfer is not compromised 妊娠糖尿病会影响胎盘、母体和脐带维生素 D 代谢物之间的相互作用，但胎儿的维生素 D 转移不会受到影响。

IF 2.5 2区医学 Q2 DEVELOPMENTAL BIOLOGY

Placenta

Pub Date : 2026-01-01 DOI: 10.1016/j.placenta.2025.03.019

Layla G. Ranquine , Deborah Bauer , Nathalia Zuniga , Brenda A. Nagagata , Gabriela D.A. Pinto , Carolina S. Ferreira , Vanessa A. Goes , Daniela B. Mucci , Lívia Belcastro , Fatima Sardinha , Claudio J. Struchiner , Alexandre G. Torres , Sarah R. Meadows , Kerry S. Jones , Tatiana El-Bacha

Introduction

The pathophysiology of gestational diabetes mellitus (GDM) is not completely understood. Poor maternal vitamin D status associates with increased risk of GDM, and placental vitamin D metabolism seems to be compromised. Here we investigated how GDM affects the associations among placental, maternal and fetal metabolism of vitamin D.

Methods

Matched placental, maternal and umbilical cord plasma samples from a clinically well-controlled cohort of pregnant women grouped into normal weight without co-morbidities (n = 8), overweight/obesity (n = 7) as the sole complication and overweight/obesity aggravated by GDM (n = 6) were analysed for vitamin D metabolites using LC-MS/MS.

Results

Maternal and cord plasma 25(OH)D₃ and 24,25(OH)₂D₃, and placental 25(OH)D₃ and vitamin D₃ were similar among the groups. Placental VDR and CYP27B1 mRNA were lower and placental-to-maternal 25(OH)D₃ ratio was higher in GDM pregnancies. In multiple regression analysis, placental 25(OH)D₃ was a positive predictor and GDM a negative predictor of maternal 25OHD₃. Importantly, GDM and overweight/obesity induced distinct maternal and placental responses in respect to vitamin D metabolism.

Discussion

GDM modified the relationship between vitamin D metabolites in cord and maternal blood, an effect possibly mediated by the placenta. Also, GDM did not affect the fetal supply of vitamin D, consistent with normal birthweight and length. The differences in metabolism possibly reflect changes in placental VDR and CYP27B1 transcripts in response to syncytiotrophoblast stress, including mitochondrial and ER stress, reported in GDM. A major limitation of this study is the small sample size which impacts on the statistical power. Thus, results should be interpreted with caution.

导言：妊娠糖尿病（GDM）的病理生理学尚不完全清楚。母体维生素 D 状态不佳与 GDM 风险增加有关，胎盘维生素 D 代谢似乎也受到影响。在此，我们研究了 GDM 如何影响胎盘、母体和胎儿的维生素 D 代谢：使用 LC-MS/MS 分析了胎盘、母体和脐带血浆样本中的维生素 D 代谢物，这些样本来自临床控制良好的孕妇队列，分为无并发症的正常体重（8 人）、作为唯一并发症的超重/肥胖（7 人）以及因 GDM 而加重的超重/肥胖（6 人）：结果：各组间母体和脐带血浆 25(OH)D3 和 24,25(OH)2D3，以及胎盘 25(OH)D3 和维生素 D3 相似。GDM孕妇的胎盘VDR和CYP27B1 mRNA较低，胎盘与母体的25（OH）D3比值较高。在多元回归分析中，胎盘 25(OH)D3 是母体 25OHD3 的正向预测因子，而 GDM 是母体 25OHD3 的负向预测因子。重要的是，在维生素 D 代谢方面，GDM 和超重/肥胖会引起不同的母体和胎盘反应：讨论：GDM改变了脐带血和母体血中维生素D代谢物之间的关系，这种影响可能是由胎盘介导的。此外，GDM 并不影响胎儿的维生素 D 供应，这与正常的出生体重和身长相符。新陈代谢的差异可能反映了胎盘 VDR 和 CYP27B1 转录物对合胞滋养细胞压力（包括线粒体和 ER 压力）反应的变化，据报道，GDM 中也存在这种变化。本研究的一个主要局限是样本量较小，影响了统计能力。因此，应谨慎解释研究结果。

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引用次数: 0

Congenital Chagas disease: The importance of Trypanosoma cruzi-placenta interactions 先天性恰加斯病：克鲁兹锥虫与胎盘相互作用的重要性。

IF 2.5 2区医学 Q2 DEVELOPMENTAL BIOLOGY

Placenta

Pub Date : 2026-01-01 DOI: 10.1016/j.placenta.2025.01.004

Castillo Christian , Liempi Ana , Fernández-Moya Alejandro , Guerrero-Muñoz Jesús , Araneda Sebastian , Cáceres Gabriela , Alfaro Sebastián , Gallardo Christian , Maya Juan Diego , Müller Marioly , Kemmerling Ulrike

引用次数: 0

Chronic mild maternal stress modulates the immune response at the maternal-fetal interface and affects the growth and mortality of the offspring 慢性轻度母体应激调节母胎界面的免疫反应，影响后代的生长和死亡率。

IF 2.5 2区医学 Q2 DEVELOPMENTAL BIOLOGY

Placenta

Pub Date : 2026-01-01 DOI: 10.1016/j.placenta.2025.10.003

F.L. De la Cruz Borthiry , J.S. Beltrame , V.A. Cañumil , F. Scheffer , M.E. Bogetti , M. Cella , M. Vermeulen , L. Gimenez , M. Negri Malbrán , E.M. Repetto , C. Cymeryng , G.F. Leguizamon , A.M. Franchi , M.L. Ribeiro

Maternal lifestyle influences the health of both the mother and fetus. Acute stress is detrimental to health and increases the risk of obstetric complications. However, the consequences of chronic mild stress are less understood. We investigated the effect of chronic mild maternal stress on gestation and its influence on the immune response at the maternal-fetal interface. BALB/c female mice were exposed to a model of mild stress involving reduced litter material compared with the control condition. Also, a shaking protocol of 1 min every other day was initiated two weeks before mating and continued until euthanasia (days 7 or 15 of pregnancy) or term labor. The stressor stimulus increased the level of serum corticosterone. Furthermore, higher concentrations of total cholesterol and triglycerides were detected in the serum of stressed pregnant mice. Stressed mothers presented lower weight gain. The offspring born to stressed mothers showed lower weight on postnatal day one, and higher early neonatal mortality. No changes were observed in the number of implantation sites, the resorption rate, ovarian architecture, and histology. However, fetuses from stressed mice exhibited lower weights. Moreover, IL-6, IL-17, and TGF-β levels increased in the amniotic fluid of stressed mothers, while no changes were detected systemically. In addition, the protein expression of TLR-4 was increased in the uterus. Moreover, cyclooxygenase-2 and prostaglandin E₂ were decreased in the placenta. In conclusion, chronic mild maternal stress induces immunological alterations at the maternal-fetal interface affecting the health of the mothers during gestation and the development of the offspring.

母亲的生活方式影响母亲和胎儿的健康。急性压力对健康有害，并增加产科并发症的风险。然而，慢性轻度压力的后果却鲜为人知。我们研究了慢性轻度母体应激对妊娠的影响及其对母胎界面免疫反应的影响。与对照组相比，BALB/c雌性小鼠暴露于轻度应激模型，其中产仔量减少。此外，在交配前两周开始每隔一天摇晃1分钟，一直持续到安乐死（怀孕第7天或第15天）或足月分娩。应激刺激使血清皮质酮水平升高。此外，在应激孕鼠血清中检测到较高浓度的总胆固醇和甘油三酯。压力大的母亲体重增加较少。压力大的母亲所生的孩子在产后第一天体重较轻，新生儿早期死亡率较高。着床部位数量、吸收率、卵巢结构和组织学均无变化。然而，应激小鼠的胎儿表现出较低的体重。此外，应激母亲羊水中IL-6、IL-17和TGF-β水平升高，但全身未见变化。此外，子宫内TLR-4蛋白表达升高。此外，环氧化酶-2和前列腺素E2在胎盘中降低。综上所述，慢性轻度母体应激诱导母胎界面的免疫改变，影响母体妊娠期的健康和后代的发育。

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引用次数: 0

Exposure to Group B Streptococcus-induced chorioamnionitis alters the proteome of placental extracellular vesicles 暴露于B组链球菌诱导的绒毛膜羊膜炎改变胎盘细胞外囊泡的蛋白质组。

IF 2.5 2区医学 Q2 DEVELOPMENTAL BIOLOGY

Placenta

Pub Date : 2026-01-01 DOI: 10.1016/j.placenta.2025.01.008

Seline Vancolen , Mathilde Chevin , Bernard Robaire , Guillaume Sébire

Introduction

Group B Streptococcus (GBS) is an opportunistic pathogen that can induce chorioamnionitis (CA), increasing the risk of neurodevelopmental disorders (NDDs) in the offspring. The placenta facilitates maternal-fetal communication through the release of extracellular vesicles (EVs), which may carry inflammatory molecules such as interleukin (IL)-1. Although the role of EVs in immune modulation is well established, their specific characterization in the context of GBS-induced CA has not yet been investigated. Understanding placental-derived EVs could further define how IL-1 and other inflammatory factors contribute to NDDs.

Methods

We used an established rat model of GBS-induced CA. EVs from control and GBS infected dams were isolated from placentas and characterized using nanoparticle tracking analysis and transmission electron microscopy. The protein content was assessed via mass spectrometry, followed by subsequent pathway analysis. ELISA was used to quantify cytokine levels.

Results

GBS-infected placentas exhibited calcification and increased weight, while fetal weight decreased. Analysis of the proteome from control versus GBS placental EVs revealed distinct profiles, with many proteins involved in the innate immune response, including alarmins (S100A8/9), complement pathways, and cytokine signaling pathways. Pathway analysis highlighted IL-1α and IL-1β identified as key upstream regulators. Notably, EVs from GBS-infected males showed a 44-fold increase in intracellular IL-1β compared to controls.

Discussion

These findings indicate that GBS-induced CA alters the protein content of EVs from placental cells. Our findings of increased IL-1β-associated EVs highlight the need for further investigation into the role of these cytokines from GBS-exposed placentas and their role in brain injuries leading to NDDs.

B群链球菌（GBS）是一种机会致病菌，可诱发绒毛膜羊膜炎（CA），增加后代发生神经发育障碍（ndd）的风险。胎盘通过释放细胞外囊泡（EVs）促进母胎通信，细胞外囊泡可能携带炎症分子，如白细胞介素(IL)-1。虽然EVs在免疫调节中的作用已经确立，但它们在gbs诱导的CA中的具体特征尚未被研究。了解胎盘源性EVs可以进一步确定IL-1和其他炎症因子如何促进ndd。方法：采用已建立的大鼠GBS诱导的CA模型，从胎盘中分离出对照和感染GBS的母鼠ev，并采用纳米颗粒跟踪分析和透射电镜对其进行表征。通过质谱法评估蛋白质含量，随后进行pathway分析。ELISA法定量细胞因子水平。结果：gbs感染的胎盘出现钙化和体重增加，胎儿体重下降。对照与GBS胎盘ev的蛋白质组分析揭示了不同的特征，许多蛋白质参与先天免疫反应，包括警报（S100A8/9）、补体途径和细胞因子信号通路。通路分析表明，IL-1α和IL-1β是关键的上游调节因子。值得注意的是，与对照组相比，来自gbs感染男性的ev显示细胞内IL-1β增加了44倍。讨论：这些发现表明，gbs诱导的CA改变了胎盘细胞EVs的蛋白质含量。我们发现il -1β相关ev增加，这表明有必要进一步研究这些细胞因子在暴露于gbs的胎盘中的作用及其在导致ndd的脑损伤中的作用。

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引用次数: 0

Association of (TG)n(GA)m repeats downstream CMA1 gene with preeclampsia in Mexican population （TG）n(GA)m重复序列下游CMA1基因与墨西哥人群子痫前期的关联

IF 2.5 2区医学 Q2 DEVELOPMENTAL BIOLOGY

Placenta

Pub Date : 2026-01-01 DOI: 10.1016/j.placenta.2025.03.018

L.J. Barragán-Zúñiga , M. Sosa-Macias , L.E. Simental-Mendía , J. Barragán-Zúñiga , B.P. Lazalde-Ramos , S. Beltrán-Ontiveros , C. Galaviz-Hernandez

Preeclampsia is a leading cause of maternal and fetal complications, often associated with endothelial dysfunction. Chymase, a proteolytic enzyme encoded by the CMA1 gene, has emerged as a potential contributor to this dysfunction. Although most preeclampsia (PE) studies have focused on maternal genetic factors, the role of paternal genetics remains underexamined. This study aimed to evaluate the association between the −1903 G/A SNV (rs1800875) and (TG)n(GA)m repeats downstream of the CMA1 gene with preeclampsia in pregnant women and their partners. A cross-sectional study was conducted involving women with PE, healthy pregnant women (HPW), and their corresponding partners, with genotyping, gene expression, and circulating protein levels assessed. A total of 141 participants were included, divided into preeclampsia (n = 80) and HPW (n = 61) groups. Women with PE showed significantly lower gestational age and higher recurrence of preeclampsia history compared to HPW. No significant association was found between the rs1800875 variant and preeclampsia; however, the (TG)n(GA)m repeat downstream of CMA1 gene was significantly associated with PE in women. Additionally, elevated serum IgE levels were significantly associated with preeclampsia (OR = 0.990; 95 % CI:0.983–0.998, p = 0.01). These findings suggest a possible role of polymorphic repeats in CMA1 as susceptibility factors for preeclampsia, indicating that both maternal and paternal genetic variations may contribute to the risk of this condition.

子痫前期是母体和胎儿并发症的主要原因，通常与内皮功能障碍有关。Chymase，一种由CMA1基因编码的蛋白水解酶，已经成为这种功能障碍的潜在贡献者。虽然大多数先兆子痫（PE）的研究都集中在母体遗传因素上，但父亲遗传的作用仍未得到充分研究。本研究旨在评估CMA1基因下游的-1903 G/A SNV （rs1800875）和（TG）n(GA)m重复序列与孕妇及其伴侣子痫前期的关系。本研究对PE患者、健康孕妇（HPW）及其伴侣进行了横断面研究，评估了基因分型、基因表达和循环蛋白水平。141名参与者被纳入研究，分为子痫前期组（n = 80）和HPW组（n = 61）。与HPW相比，PE患者的胎龄明显较低，子痫前期复发率较高。rs1800875变异与子痫前期无显著相关性；然而，CMA1基因下游的（TG）n(GA)m重复序列与女性PE显著相关。此外，血清IgE水平升高与子痫前期显著相关(OR = 0.990；95% CI:0.983 ~ 0.998, p = 0.01)。这些发现表明CMA1多态性重复序列可能是子痫前期的易感性因素，表明母亲和父亲的遗传变异都可能导致这种情况的风险。

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引用次数: 0

Cytotoxicity and induction of proinflammatory cytokines in placental explant cells following azathioprine exposure 硫唑嘌呤暴露后胎盘外植体细胞的细胞毒性和促炎细胞因子的诱导。

IF 2.5 2区医学 Q2 DEVELOPMENTAL BIOLOGY

Placenta

Pub Date : 2026-01-01 DOI: 10.1016/j.placenta.2025.05.002

Franciele Rodrigues Araújo , Adriana Lopes da Silva , Leandro de Oliveira , Simone Correa-Silva , Estela Bevilacqua

Immunosuppressive drugs offer hope for the survival and motherhood of women with various disorders. Although the systemic side effects of these drugs on mothers have been studied, their impact on the placenta remains poorly understood, which can negatively affect fetal and postnatal development. This study investigated the effects of Azathioprine, an immunosuppressive drug, on the chorionic villi of human placentas from healthy pregnancies, focusing on cellular vitality and pro-inflammatory cytokines expression. Chorionic villi from term placentas were cultured and treated with Azathioprine at concentrations ranging from 0 to 100 ng/mL for 24 h. Azathioprine reduced mitochondrial metabolic activity (MTT assay) at all concentrations tested (p < 0.05) and increased cellular injury rates (LDH assay) at 50 and 100 ng/mL (p < 0.05). It also elevated protein (at 12.5 and 25 ng/mL, p < 0.05) and gene expression levels of interleukin (IL)-1β (12.5 ng/mL, p < 0.05). Protein levels of IL-18 increased significantly following Azathioprine exposure (p < 0.05), along with cleaved Caspase-1 (p = 0.003) and phosphorylated NF-κB levels (p < 0.05), compared to controls. IL-18 gene expression was elevated only at 12.5 ng/mL (p < 0.0005). These findings suggest that Azathioprine creates a cytotoxic microenvironment that disrupts the metabolism of chorionic villi, leading to injury and activation of pro-inflammatory cytokine expression. Such changes may contribute to an imbalance in placental homeostasis, potentially associated with adverse maternal and neonatal outcomes that warrant further investigation.

免疫抑制药物为患有各种疾病的妇女的生存和生育带来了希望。虽然已经研究了这些药物对母亲的全身副作用，但它们对胎盘的影响仍然知之甚少，这可能对胎儿和产后发育产生负面影响。本研究探讨了免疫抑制药物硫唑嘌呤对健康妊娠人胎盘绒毛膜绒毛的影响，重点关注细胞活力和促炎细胞因子的表达。将足月胎盘的绒毛膜绒毛培养，并用浓度为0至100 ng/mL的硫唑嘌呤处理24小时。硫唑嘌呤在所有浓度下都降低了线粒体代谢活性（MTT测定）

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引用次数: 0

Exploring the role of specialized pro-resolving mediators, fatty acid oxidation markers and transporters in Gestational Diabetes Mellitus (GDM) placentae 探讨特殊促溶解介质、脂肪酸氧化标记物和转运体在妊娠糖尿病（GDM）胎盘中的作用。

IF 2.5 2区医学 Q2 DEVELOPMENTAL BIOLOGY

Placenta

Pub Date : 2025-12-29 DOI: 10.1016/j.placenta.2025.12.014

Nikita Joshi , Deepali Sundrani , Hemlata Pisal , Karuna Randhir , Girija Wagh , Sanjay Lalwani , Sanjay Gupte , Sadhana Joshi

Background

The role of fatty acids is critical throughout pregnancy and can influence pregnancy outcome. Materno-fetal transfer of fatty acids depends on placental fatty acid metabolism which includes fatty acid specialized pro-resolving mediators (SPMs) production, activation of peroxisome proliferated activated receptors (PPARs) and fatty acid oxidation. Alterations in any of these mechanisms may influence fetal development. This study reports placental levels of SPMs (protectins and lipoxins), PPARα, fatty acid oxidation marker (CPT1A) and fatty acid transporters (FATP1 and FATP4) in GDM and non-GDM women.

Methods

The study included 209 women with GDM and 207 non-GDM women. The levels of protectins, lipoxins, PPARα, CPT1A, FATP1 and FATP4 were estimated using ELISA kits from placental tissue homogenates. The placental gene expression of PPARα, CPT1A, FATP1 and FATP4 was examined using quantitative real time PCR. Pearson's correlation was used to explore the association between these placental markers.

Results

The placental protectin D1 (PD1; p < 0.05) was decreased whereas the lipoxin A4 (LXA4; p < 0.01), CPT1A, FATP1 and FATP4 (p < 0.05; for all) were increased in GDM as compared to non-GDM. The mRNA expression of PPARα, CPT1A, FATP1 and FATP4 were comparable between groups. The LXA4 and PD1 were positively correlated with PPARα (p < 0.01; for both). There was a positive association of PPARα with CPT1A, FATP1 and FATP4 (p < 0.01; for all).

Conclusion

Specialized pro-resolving mediators, fatty acid oxidation markers and fatty acid transporters are altered in GDM placentae.

背景：脂肪酸在整个妊娠过程中起着至关重要的作用，并可能影响妊娠结局。脂肪酸的母胎转移依赖于胎盘脂肪酸代谢，包括脂肪酸特异性促分解介质（SPMs）的产生、过氧化物酶体增殖活化受体（ppar）的激活和脂肪酸氧化。这些机制的任何改变都可能影响胎儿发育。本研究报道了GDM和非GDM女性胎盘中SPMs（保护素和脂毒素）、PPARα、脂肪酸氧化标志物（CPT1A）和脂肪酸转运蛋白（FATP1和FATP4）的水平。方法：研究对象为209例GDM女性和207例非GDM女性。利用ELISA试剂盒检测胎盘组织匀浆中保护蛋白、脂毒素、PPARα、CPT1A、FATP1和FATP4的水平。采用实时荧光定量PCR检测胎盘中PPARα、CPT1A、FATP1和FATP4基因的表达。Pearson相关性被用来探索这些胎盘标记物之间的关联。结果：胎盘保护素D1 （PD1; p）在GDM胎盘中发生改变。结论：GDM胎盘中特异性促分解介质、脂肪酸氧化标志物和脂肪酸转运蛋白发生改变。

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引用次数: 0

Histopathologic changes of the placenta in Q fever infection: An Australian case series Q热感染中胎盘的组织病理学改变：一个澳大利亚病例系列

IF 2.5 2区医学 Q2 DEVELOPMENTAL BIOLOGY

Placenta

Pub Date : 2025-12-29 DOI: 10.1016/j.placenta.2025.12.015

Lucinda Taege , Mark Armstrong , Vichitra Sukumaran , Robert Horvath

Objectives

Q fever is a zoonotic infectious disease with a particular tropism for the placenta. Some studies have suggested associated adverse outcomes including intrauterine growth restriction (IUGR) and intrauterine fetal demise (IUFD). Despite this, data on corresponding histologic features of the placenta are sparse. The aim of this study was to describe histopathologic findings of the placenta in cases of Q fever infection with their associated pregnancy outcomes.

Methods

Patients were identified in a database search of Queensland cases between January 2000 and January 2025. The study was inclusive of all patients with a confirmed diagnosis of Q fever through serological or PCR testing, and placental histopathology performed. Histopathologic features of the placenta were reviewed and described based on slides and reports. Epidemiologic, clinical and microbiologic data was also extracted and described.

Results

Ten patients were identified, including four asymptomatic infections, two partially treated infections, and four treated infections. PCR testing of the placenta was performed in all cases, and was positive in all untreated infections, and one partially treated infection. These PCR positive cases showed distinct findings, with a florid acute villitis and intervillositis, abscess formation and decidual necrosis. One partially treated infection showed atypical features including a chronic villitis and chorionic plate inflammation with giant cells. The treated and placental PCR negative cases did not show any specific abnormalities.

Conclusions

This study finds a specific histologic appearance associated with untreated Q fever infection and poor outcomes in pregnancy. The histologic findings described should prompt reflex Q fever testing.

目的q热是一种以胎盘为特征性的人畜共患传染病。一些研究表明相关的不良后果包括宫内生长受限（IUGR）和宫内胎儿死亡（IUFD）。尽管如此，关于胎盘的相应组织学特征的数据很少。本研究的目的是描述Q热感染病例胎盘的组织病理学结果及其相关的妊娠结局。方法通过2000年1月至2025年1月间昆士兰州病例数据库检索患者。该研究包括所有通过血清学或PCR检测确诊为Q热的患者，并进行了胎盘组织病理学检查。根据幻灯片和报告对胎盘的组织病理学特征进行了回顾和描述。还提取和描述了流行病学、临床和微生物学数据。结果共发现10例患者，其中无症状感染4例，部分治疗感染2例，治疗感染4例。所有病例均进行了胎盘PCR检测，所有未经治疗的感染和1例部分治疗的感染均呈阳性。这些PCR阳性的病例表现出明显的症状，有丰富的急性绒毛炎和绒毛间炎，脓肿形成和蜕膜坏死。一个部分治疗的感染表现出非典型特征，包括慢性绒毛炎和巨细胞绒毛膜板炎症。经治疗和胎盘PCR阴性的病例未显示任何特异性异常。结论：本研究发现了一种与未经治疗的Q热感染和妊娠不良结局相关的特殊组织学表现。所描述的组织学结果应提示反射性Q热检测。

{"title":"Histopathologic changes of the placenta in Q fever infection: An Australian case series","authors":"Lucinda Taege , Mark Armstrong , Vichitra Sukumaran , Robert Horvath","doi":"10.1016/j.placenta.2025.12.015","DOIUrl":"10.1016/j.placenta.2025.12.015","url":null,"abstract":"<div><h3>Objectives</h3><div>Q fever is a zoonotic infectious disease with a particular tropism for the placenta. Some studies have suggested associated adverse outcomes including intrauterine growth restriction (IUGR) and intrauterine fetal demise (IUFD). Despite this, data on corresponding histologic features of the placenta are sparse. The aim of this study was to describe histopathologic findings of the placenta in cases of Q fever infection with their associated pregnancy outcomes.</div></div><div><h3>Methods</h3><div>Patients were identified in a database search of Queensland cases between January 2000 and January 2025. The study was inclusive of all patients with a confirmed diagnosis of Q fever through serological or PCR testing, and placental histopathology performed. Histopathologic features of the placenta were reviewed and described based on slides and reports. Epidemiologic, clinical and microbiologic data was also extracted and described.</div></div><div><h3>Results</h3><div>Ten patients were identified, including four asymptomatic infections, two partially treated infections, and four treated infections. PCR testing of the placenta was performed in all cases, and was positive in all untreated infections, and one partially treated infection. These PCR positive cases showed distinct findings, with a florid acute villitis and intervillositis, abscess formation and decidual necrosis. One partially treated infection showed atypical features including a chronic villitis and chorionic plate inflammation with giant cells. The treated and placental PCR negative cases did not show any specific abnormalities.</div></div><div><h3>Conclusions</h3><div>This study finds a specific histologic appearance associated with untreated Q fever infection and poor outcomes in pregnancy. The histologic findings described should prompt reflex Q fever testing.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"174 ","pages":"Pages 196-202"},"PeriodicalIF":2.5,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145883731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Complement factor H-point mutation promotes the development of preeclampsia-like phenotype with multiparity in mice 补体因子h点突变促进小鼠多胎子痫样表型的发展。

IF 2.5 2区医学 Q2 DEVELOPMENTAL BIOLOGY

Placenta

Pub Date : 2025-12-25 DOI: 10.1016/j.placenta.2025.12.010

Fei-fei Chen , Zheng Li , Ying Tan , Hui Wang , Shi Chen , Feng Yu , Ying-dong He , Qian Chen , Hui-xia Yang , Ming-hui Zhao

Introduction

Preeclampsia, a severe pregnancy disorder associated with the placenta, remains incompletely understood in terms of its pathogenesis. Studies have suggested a link between complement activation and preeclampsia. In normal pregnancy, there is a moderate balance between complement-activating factor and regulatory protein. Fourteen percent of patients with preeclampsia/hemolysis, elevated liver enzymes and low platelet syndrome (HELLP syndrome) have a genetic mutation in complement regulators, leading to impaired regulation of the alternative complement pathway. However, the direct association between this and the precise role of pregnancy in triggering preeclampsia via complement system activation remains elusive.

Methods

Here, we evaluated the clinicopathological characteristics of preeclampsia in female mice harboring heterozygous mutations in complement factor H (CFH) (FH^W/R). Blood pressure, 24-h urine protein, blood biochemistry, routine blood tests, circulating complement activation factors, placental pathology, local complement activation and vascular activation were detected in both groups of mice.

Results

Along with complement activation, these mice manifested hallmark features of human preeclampsia, including hypertension, proteinuria, increased lactic dehydrogenase, reduced placental weight, restricted fetal growth, characteristic histological alterations in the placenta and kidney, disrupted placental angiogenesis and renal endothelial cell injury.

Conclusions

We induced the key features of human preeclampsia in mice with heterozygous mutations in complement factor H,which suggest that individuals with increased genetic susceptibility to complement system overactivation may constitute a population which may have an increased risk to develop preeclampsia like phenotype of hypertension.

先兆子痫是一种与胎盘相关的严重妊娠疾病，其发病机制尚不完全清楚。研究表明补体激活和先兆子痫之间存在联系。在正常妊娠中，补体活化因子与调节蛋白之间存在适度的平衡。14%的先兆子痫/溶血、肝酶升高和低血小板综合征（HELLP综合征）患者在补体调节因子中存在基因突变，导致替代补体途径的调节受损。然而，这与妊娠通过补体系统激活引发子痫前期的确切作用之间的直接联系仍然难以捉摸。方法：对补体因子H (CFH) （FHW/R）杂合突变雌性小鼠子痫前期的临床病理特征进行评价。检测两组小鼠血压、24小时尿蛋白、血生化、血常规、循环补体活化因子、胎盘病理、局部补体活化、血管活化。结果：随着补体激活，这些小鼠表现出人类子痫前期的标志性特征，包括高血压、蛋白尿、乳酸脱氢酶升高、胎盘重量减轻、胎儿生长受限、胎盘和肾脏的特征性组织学改变、胎盘血管生成中断和肾内皮细胞损伤。结论：我们在补体因子H杂合突变的小鼠中诱导了人类子痫前期的关键特征，这表明对补体系统过度激活的遗传易感性增加的个体可能构成了一个可能有更高风险发展为子痫前期样高血压表型的人群。

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引用次数: 0