313. Fetal microchimerism in pregnancy and placental dysfunction

2018 ◽  
Vol 13 ◽  
pp. S122 ◽  
Author(s):  
Heidi E. Fjeldstad ◽  
Anne Cathrine Staff ◽  
Angel Chae ◽  
Christopher Redman ◽  
Hilary S. Gammill ◽  
...  
2008 ◽  
Vol 1 (2) ◽  
pp. 56-64 ◽  
Author(s):  
Keelin O'Donoghue

Trafficking of fetal cells into the maternal circulation begins very early in pregnancy and the effects of this cell traffic are longlasting. All types of fetal cells, including stem cells, cross the placenta during normal pregnancy to enter maternal blood, from where they may be recovered in pregnancy for the purpose of genetic prenatal diagnosis. Fetal cells can also be located in maternal tissues during and after pregnancy, and persist as microchimeric cells for decades in marrow and other organs. Although persistent fetal cells were first implicated in autoimmune disease, subsequent reports routinely found microchimeric cells in healthy tissues and in non-autoimmune disease. Parallel studies in animal and human pregnancy now suggest instead that microchimeric fetal cells play a role in the response to tissue injury. However, it is still not clear whether microchimeric fetal cells persisting in the mother are an incidental finding, are naturally pathogenic or act as reparative stem cells, and the environmental or biological stimuli that determine microchimeric cell fate are as yet undetermined. Future studies must also focus on investigating whether fetal cells create functional improvement in response to maternal injury and whether this response can be manipulated. The pregnancy-acquired low-grade chimeric state of women could have far-reaching implications, influencing recovery after injury or surgery, ageing, graft survival after transplantation, survival after cancer as well as deciding the protective effect of pregnancy against diseases later in life. Lifelong persistence of fetal cells in maternal tissues may even explain why women live longer than men.


2021 ◽  
Vol 22 (19) ◽  
pp. 10732
Author(s):  
Désirée Forstner ◽  
Jacqueline Guettler ◽  
Martin Gauster

Upon activation, maternal platelets provide a source of proinflammatory mediators in the intervillous space of the placenta. Therefore, platelet-derived factors may interfere with different trophoblast subtypes of the developing human placenta and might cause altered hormone secretion and placental dysfunction later on in pregnancy. Increased platelet activation, and the subsequent occurrence of placental fibrinoid deposition, are linked to placenta pathologies such as preeclampsia. The composition and release of platelet-derived factors change over gestation and provide a potential source of predicting biomarkers for the developing fetus and the mother. This review indicates possible mechanisms of platelet-trophoblast interactions and discusses the effect of increased platelet activation on placenta development.


2019 ◽  
Vol 97 (3) ◽  
pp. 206-212 ◽  
Author(s):  
Marie-Eve Brien ◽  
Bernadette Baker ◽  
Cyntia Duval ◽  
Virginie Gaudreault ◽  
Rebecca L. Jones ◽  
...  

Inflammation is known to be associated with placental dysfunction and pregnancy complications. Infections are well known to be a cause of inflammation but they are frequently undetectable in pregnancy complications. More recently, the focus has been extended to inflammation of noninfectious origin, namely caused by endogenous mediators known as “damage-associated molecular patterns (DAMPs)” or alarmins. In this manuscript, we review the mechanism by which inflammation, sterile or infectious, can alter the placenta and its function. We discuss some classical DAMPs, such as uric acid, high mobility group box 1 (HMGB1), cell-free fetal deoxyribonucleic acid (DNA) (cffDNA), S100 proteins, heat shock protein 70 (HSP70), and adenosine triphosphate (ATP) and their impact on the placenta. We focus on the main placental cells (i.e., trophoblast and Hofbauer cells) and describe the placental response to, and release of, DAMPs. We also covered the current state of knowledge about the role of DAMPs in pregnancy complications including preeclampsia, fetal growth restriction, preterm birth, and stillbirth and possible therapeutic strategies to preserve placental function.


2019 ◽  
Vol 17 ◽  
pp. S14
Author(s):  
Heidi E.S. Fjeldstad ◽  
Guro M. Johnsen ◽  
Kjartan Moe ◽  
Angel Chae ◽  
Patji Alnæs-Katjavivi ◽  
...  

Endocrinology ◽  
2002 ◽  
Vol 143 (1) ◽  
pp. 247-253 ◽  
Author(s):  
M. Imaizumi ◽  
A. Pritsker ◽  
P. Unger ◽  
T. F. Davies

Medicina ◽  
2021 ◽  
Vol 57 (4) ◽  
pp. 390
Author(s):  
Filipe Benito-Garcia ◽  
Inês Pires ◽  
Jorge Lima

Low-dose acetylsalicylic acid (ASA) is widely used during pregnancy to prevent obstetric complications of placental dysfunction, such as preeclampsia, stillbirth and fetal growth restriction, and obstetric complications in pregnant women with antiphospholipid syndrome. ASA-sensitive pregnant women cannot benefit from the effects of ASA due to the possibility of severe or potentially life-threatening hypersensitivity reactions to ASA. ASA desensitization is a valuable and safe therapeutic option for these women, allowing them to start daily prophylaxis with ASA and prevent pregnancy complications. The authors discuss the recent advances in obstetric conditions preventable by ASA and the management of ASA hypersensitivity in pregnancy, including ASA desensitization. To encourage the implementation of ASA desensitization protocols in ASA-sensitive pregnant women, they also propose a practical approach for use in daily clinical practice.


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