scholarly journals Influence of infection during pregnancy on fetal development

Reproduction ◽  
2013 ◽  
Vol 146 (5) ◽  
pp. R151-R162 ◽  
Author(s):  
Kristina M Adams Waldorf ◽  
Ryan M McAdams
Keyword(s):  
Oxidative Stress ◽  
Fetal Growth ◽  
Fetal Development ◽  
Parvovirus B19 ◽  
Treponema Pallidum ◽  
In Utero ◽  
Organ Injury ◽  
Placental Development ◽  
Varicella Zoster

Infection by bacteria, viruses, and parasites may lead to fetal death, organ injury, or limited sequelae depending on the pathogen. Here, we consider the role of infection during pregnancy in fetal development including placental development and function, which can lead to fetal growth restriction. The classical group of teratogenic pathogens is referred to as ‘TORCH’ (Toxoplasma gondii, others likeTreponema pallidum, rubella virus, cytomegalovirus, and herpes simplex virus) but should include a much broader group of pathogens including Parvovirus B19,Varicella zostervirus, andPlasmodium falciparumto name a few. In this review, we describe the influence of different infectionsin uteroon fetal development and the short- and long-term outcomes for the neonate. In some cases, the mechanisms used by these pathogens to disrupt fetal development are well known. Bacterial infection of the developing fetal lungs and brain begins with an inflammatory cascade resulting in cytokine injury and oxidative stress. For some pathogens likeP.falciparum, the mechanisms involve oxidative stress and apoptosis to disrupt placental and fetal growth. Anin uteroinfection may also affect the long-term health of the infant; in many cases, a viral infectionin uteroincreases the risk of developing type 1 diabetes in childhood. Understanding the varied mechanisms employed by these pathogens may enable therapies to attenuate changes in fetal development, decrease preterm birth, and improve survival.

scholarly journals Endocrine mechanisms of intrauterine programming

Reproduction ◽  
2004 ◽  
Vol 127 (5) ◽  
pp. 515-526 ◽  
Author(s):  
A L Fowden ◽  
A J Forhead
Keyword(s):  
Growth Factors ◽  
Fetal Growth ◽  
Fetal Development ◽  
Experimental Studies ◽  
In Utero ◽  
Tissue Growth ◽  
Postnatal Life ◽  
Organ Systems ◽  
Intrauterine Programming

Epidemiological findings and experimental studies in animals have shown that individual tissues and whole organ systems can be programmedin uteroduring critical periods of development with adverse consequences for their function in later life. Detailed morphometric analyses of the data have shown that certain patterns of intrauterine growth, particularly growth retardation, can be related to specific postnatal outcomes. Since hormones regulate fetal growth and the development of individual fetal tissues, they have a central role in intrauterine programming. Hormones such as insulin, insulin-like growth factors, thyroxine and the glucocorticoids act as nutritional and maturational signals and adapt fetal development to prevailing intrauterine conditions, thereby maximizing the chances of survival bothin uteroand at birth. However, these adaptations may have long-term sequelae. Of the hormones known to control fetal development, it is the glucocorticoids that are most likely to cause tissue programmingin utero. They are growth inhibitory and affect the development of all the tissues and organ systems most at risk of postnatal pathophysiology when fetal growth is impaired. Their concentrationsin uteroare also elevated by all the nutritional and other challenges known to have programming effects. Glucocorticoids act at cellular and molecular levels to alter cell function by changing the expression of receptors, enzymes, ion channels and transporters. They also alter various growth factors, cytoarchitectural proteins, binding proteins and components of the intracellular signalling pathways. Glucocorticoids act, directly, on genes and, indirectly, through changes in the bioavailability of other hormones. These glucocorticoid-induced endocrine changes may be transient or persist into postnatal life with consequences for tissue growth and development both before and after birth. In the long term, prenatal glucocorticoid exposure can permanently reset endocrine systems, such as the somatotrophic and hypothalamic–pituitary–adrenal axes, which, in turn, may contribute to the pathogenesis of adult disease. Endocrine changes may, therefore, be both the cause and the consequence of intrauterine programming.

Maternal Oxidative Stress, Placental Morphometry, and Fetal Growth in Diabetic Rats Exposed to Cigarette Smoke

2018 ◽  
Vol 26 (9) ◽  
pp. 1287-1293 ◽  
Author(s):  
Yuri K. Sinzato ◽  
Estela M. Bevilacqua ◽  
Gustavo T. Volpato ◽  
Rogelio E. Hernandez-Pando ◽  
Marilza V. C. Rudge ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Fetal Growth ◽  
Fetal Development ◽  
Oxidative Stress Biomarkers ◽  
Junctional Zone ◽  
Pregnant Rats ◽  
Stress Biomarkers ◽  
Vascular Walls ◽  
The Impact

The diabetic syndrome affects pregnancy, contributing to placental functional and structural disruptions and impaired fetal development, with many reports indicating tobacco-associated morbidity and perinatal mortality. In our study, an experimental rat model of diabetes and cigarette smoke exposure in pregnant rats was used to determine the impact of the combination of diabetes and exposure to cigarette smoke during pregnancy on maternal oxidative stress biomarkers and placental and fetal development. Diabetes was induced by streptozotocin, and dams were exposed to cigarette smoke by mainstream smoke generated by a mechanical smoking device and delivered into a chamber. Four groups of dams were studied: nondiabetic (C, control) and diabetic (D) exposed to filtered air and nondiabetic (CS) and diabetic (DS) exposed to cigarette smoke prior to and during pregnancy. Maternal oxidative stress biomarkers, placental morphology, and fetal growth were determined close to term. The combination of diabetes and cigarette smoke resulted in elevated maternal blood glucose levels and increased number of small fetuses. Placentas from the DS group showed increased junctional zone and decreased labyrinthine area. The morphological alterations were characterized by extensive vascular congestion, thickness, and hyalinization of the vascular walls, numerous decidual cells with abundant glycogen, and macrophages with cytoplasmic inclusions of hemosiderin. Additionally, they showed increased glycogen accumulation and junctional zone structural derangement with ectopic giant cells. No alterations were observed in maternal oxidative stress status. Thus, our result suggests that diabetes makes pregnant rats more susceptible to the adverse effects of exposure to cigarette smoke on placental morphometry and fetal growth.

scholarly journals The Role of NFκB in Healthy and Preeclamptic Placenta: Trophoblasts in the Spotlight

2020 ◽  
Vol 21 (5) ◽  
pp. 1775 ◽  
Author(s):  
Brooke Armistead ◽  
Leena Kadam ◽  
Sascha Drewlo ◽  
Hamid-Reza Kohan-Ghadr
Keyword(s):  
Oxidative Stress ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Growth And Development ◽  
Protein Family ◽  
Growth Restriction ◽  
Placental Development ◽  
Critical Organ ◽  
And Oxidative Stress

The NFκB protein family regulates numerous pathways within the cell—including inflammation, hypoxia, angiogenesis and oxidative stress—all of which are implicated in placental development. The placenta is a critical organ that develops during pregnancy that primarily functions to supply and transport the nutrients required for fetal growth and development. Abnormal placental development can be observed in numerous disorders during pregnancy, including fetal growth restriction, miscarriage, and preeclampsia (PE). NFκB is highly expressed in the placentas of women with PE, however its contributions to the syndrome are not fully understood. In this review we discuss the molecular actions and related pathways of NFκB in the placenta and highlight areas of research that need attention

Ultrasound Aspects of Fetal and Extrafetal Structures in Pregnant Cats

2002 ◽  
Vol 4 (2) ◽  
pp. 95-106 ◽  
Author(s):  
D Zambelli ◽  
B Caneppele ◽  
S Bassi ◽  
C Paladini
Keyword(s):  
Fetal Growth ◽  
Fetal Development ◽  
Ultrasound Examination ◽  
Crystalline Lens ◽  
Fetal Membranes ◽  
Ultrasound Images ◽  
Placental Development ◽  
Ultrasound Scanner

Prenatal feline fetal growth and utero-placental development were ultrasonographically evaluated using an ultrasound scanner with a 10 MHz sector probe. Uterus, placenta, embryo, fetus and fetal membranes in 16 pregnant cats were monitored during the course of pregnancy; 13 subjects underwent an ovariectomy on specific days while three subjects went to term. Various anatomic structures, fixed in Carson-buffered formalin, were sectioned and then compared to ultrasound images. By ultrasound examination it is possible to evaluate every stage of the fetal development; the gestational chamber can be seen on the 10th and the embryo inside the chamber on the 14th day. By the 20th day it is possible to evaluate all the fetal membranes, and later it is possible to appreciate organs and structures such as the stomach, intestine, eyes (crystalline lens), kidneys and the cerebral choroid plexi, on the 30th, 40th, 50th, 39th and 40th day respectively. Based on our observations, it will be simpler to locate anomalies of development or pathologies during ultrasound examination of pregnant queens.

scholarly journals The application of in utero magnetic resonance imaging in the study of the metabolic and cardiovascular consequences of the developmental origins of health and disease

2020 ◽  
pp. 1-10
Author(s):  
Stephanie A. Giza ◽  
Simran Sethi ◽  
Lauren M. Smith ◽  
Mary-Ellen E. T. Empey ◽  
Lindsay E. Morris ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Adipose Tissue ◽  
Magnetic Resonance ◽  
Fetal Growth ◽  
Fetal Development ◽  
In Utero ◽  
Developmental Origins ◽  
Organ Development ◽  
Resonance Imaging ◽  
Health And Disease

Abstract Observing fetal development in utero is vital to further the understanding of later-life diseases. Magnetic resonance imaging (MRI) offers a tool for obtaining a wealth of information about fetal growth, development, and programming not previously available using other methods. This review provides an overview of MRI techniques used to investigate the metabolic and cardiovascular consequences of the developmental origins of health and disease (DOHaD) hypothesis. These methods add to the understanding of the developing fetus by examining fetal growth and organ development, adipose tissue and body composition, fetal oximetry, placental microstructure, diffusion, perfusion, flow, and metabolism. MRI assessment of fetal growth, organ development, metabolism, and the amount of fetal adipose tissue could give early indicators of abnormal fetal development. Noninvasive fetal oximetry can accurately measure placental and fetal oxygenation, which improves current knowledge on placental function. Additionally, measuring deficiencies in the placenta’s transport of nutrients and oxygen is critical for optimizing treatment. Overall, the detailed structural and functional information provided by MRI is valuable in guiding future investigations of DOHaD.

Long-term effects of nutritional programming of the embryo and fetus: mechanisms and critical windows

2007 ◽  
Vol 19 (1) ◽  
pp. 53 ◽  
Author(s):  
Michael E. Symonds ◽  
Terence Stephenson ◽  
David S. Gardner ◽  
Helen Budge
Keyword(s):  
Fetal Growth ◽  
Epidemiological Studies ◽  
Maternal Plasma ◽  
Metabolic Effects ◽  
Global Changes ◽  
Long Term Effects ◽  
Placental Development ◽  
Increased Risk ◽  
Large Animals

The maternal nutritional and metabolic environment is critical in determining not only reproduction, but also long-term health and viability. In the present review, the effects of maternal nutritional manipulation at defined stages of gestation coinciding with embryogenesis, maximal placental or fetal growth will be discussed. Long-term outcomes from these three developmental windows appear to be very different, with brain and cardiovascular function being most sensitive to influences in the embryonic period, the kidney during placental development and adipose tissue in the fetal phase. In view of the similarities in fetal development, number and maturity at birth, there are close similarities in these outcomes between findings from epidemiological studies in historical human cohorts and nutritional manipulation of large animals, such as sheep. One key nutrient that may modulate the long-term metabolic effects is the supply of glucose from the mother to the fetus, because this is sensitive to both global changes in food intake, maternal glucocorticoid status and an increase in the carbohydrate content of the diet. The extent to which these dietary-induced changes may reflect epigenetic changes remains to be established, especially when considering the very artificial diets used to induce these types of effects. In summary, the maintenance of a balanced and appropriate supply of glucose from the mother to the fetus may be pivotal in ensuring optimal embryonic, placental and fetal growth. Increased or decreased maternal plasma glucose alone, or in conjunction with other macro- or micronutrients, may result in offspring at increased risk of adult diseases.

scholarly journals In-utero stress and mode of conception: impact on regulation of imprinted genes, fetal development and future health

2019 ◽  
Vol 25 (6) ◽  
pp. 777-801 ◽  
Author(s):  
Maria Argyraki ◽  
Pauliina Damdimopoulou ◽  
Katerina Chatzimeletiou ◽  
Grigoris F Grimbizis ◽  
Basil C Tarlatzis ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Psychological Stress ◽  
Genomic Imprinting ◽  
Fetal Growth ◽  
Fetal Development ◽  
Environmental Chemicals ◽  
Imprinted Genes ◽  
Epigenetic Patterns

AbstractBACKGROUNDGenomic imprinting is an epigenetic gene regulatory mechanism; disruption of this process during early embryonic development can have major consequences on both fetal and placental development. The periconceptional period and intrauterine life are crucial for determining long-term susceptibility to diseases. Treatments and procedures in assisted reproductive technologies (ART) and adverse in-utero environments may modify the methylation levels of genomic imprinting regions, including insulin-like growth factor 2 (IGF2)/H19, mesoderm-specific transcript (MEST), and paternally expressed gene 10 (PEG10), affecting the development of the fetus. ART, maternal psychological stress, and gestational exposures to chemicals are common stressors suspected to alter global epigenetic patterns including imprinted genes.OBJECTIVE AND RATIONALEOur objective is to highlight the effect of conception mode and maternal psychological stress on fetal development. Specifically, we monitor fetal programming, regulation of imprinted genes, fetal growth, and long-term disease risk, using the imprinted genes IGF2/H19, MEST, and PEG10 as examples. The possible role of environmental chemicals in genomic imprinting is also discussed.SEARCH METHODSA PubMed search of articles published mostly from 2005 to 2019 was conducted using search terms IGF2/H19, MEST, PEG10, imprinted genes, DNA methylation, gene expression, and imprinting disorders (IDs). Studies focusing on maternal prenatal stress, psychological well-being, environmental chemicals, ART, and placental/fetal development were evaluated and included in this review.OUTCOMESIGF2/H19, MEST, and PEG10 imprinted genes have a broad developmental effect on fetal growth and birth weight variation. Their disruption is linked to pregnancy complications, metabolic disorders, cognitive impairment, and cancer. Adverse early environment has a major impact on the developing fetus, affecting mostly growth, the structure, and subsequent function of the hypothalamic–pituitary–adrenal axis and neurodevelopment. Extensive evidence suggests that the gestational environment has an impact on epigenetic patterns including imprinting, which can lead to adverse long-term outcomes in the offspring. Environmental stressors such as maternal prenatal psychological stress have been found to associate with altered DNA methylation patterns in placenta and to affect fetal development. Studies conducted during the past decades have suggested that ART pregnancies are at a higher risk for a number of complications such as birth defects and IDs. ART procedures involve multiple steps that are conducted during critical windows for imprinting establishment and maintenance, necessitating long-term evaluation of children conceived through ART. Exposure to environmental chemicals can affect placental imprinting and fetal growth both in humans and in experimental animals. Therefore, their role in imprinting should be better elucidated, considering the ubiquitous exposure to these chemicals.WIDER IMPLICATIONSDysregulation of imprinted genes is a plausible mechanism linking stressors such as maternal psychological stress, conception using ART, and chemical exposures with fetal growth. It is expected that a greater understanding of the role of imprinted genes and their regulation in fetal development will provide insights for clinical prevention and management of growth and IDs. In a broader context, evidence connecting impaired imprinted gene function to common diseases such as cancer is increasing. This implies early regulation of imprinting may enable control of long-term human health, reducing the burden of disease in the population in years to come.

INTRAUTERINE GROWTH RETARDATION - A REVIEW ARTICLE

2018 ◽  
pp. 184-195
Author(s):  
Minh Son Pham ◽  
Vu Quoc Huy Nguyen ◽  
Dinh Vinh Tran
Keyword(s):  
Fetal Growth ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Growth Potential ◽  
National Guidelines ◽  
Intrauterine Growth ◽  
No Gold Standard

Small for gestational age (SGA) and fetal growth restriction (FGR) is difficult to define exactly. In this pregnancy condition, the fetus does not reach its biological growth potential as a consequence of impaired placental function, which may be because of a variety of factors. Fetuses with FGR are at risk for perinatal morbidity and mortality, and poor long-term health outcomes, such as impaired neurological and cognitive development, and cardiovascular and endocrine diseases in adulthood. At present no gold standard for the diagnosis of SGA/FGR exists. The first aim of this review is to: summarize areas of consensus and controversy between recently published national guidelines on small for gestational age or fetal growth restriction; highlight any recent evidence that should be incorporated into existing guidelines. Another aim to summary a number of interventions which are being developed or coming through to clinical trial in an attempt to improve fetal growth in placental insufficiency. Key words: fetal growth restriction (FGR), Small for gestational age (SGA)

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