Development Of Offspring Research Articles

Placental transcriptome variation associated with season, location, and urinary prenatal pyrethroid metabolites of Thai farm-working women

Prenatal exposure to pyrethroids is linked to adverse health effects in early life and proper placental function is critical to fetal development. This study explores the impact of prenatal pyrethroid exposure, as well as factors impacting exposure and effect, on the placental transcriptome, to understand pyrethroid exposures' relationship to placental function. The study of Asian Women and their Offspring's Development and Environmental Exposures (SAWASDEE) recruited pregnant farm-working women from two agricultural districts in the Chiang Mai province of Thailand between 2017 and 2019. This cohort was predominantly exposed to cypermethrin (type II), alongside pyrethroids such as cyfluthrin (type II) and permethrin (type I). In 253 participants, maternal urinary pyrethroid metabolites, 3-phenoxybenzoic acid (PBA), cis-3-(2,2-Dichlorovinyl)-2,2-dimethylcyclopropane carboxylic acid (CDCCA), and trans-3-(2,2-Dichlorovinyl)-2,2-dimethylcyclopropane carboxylic acid (TDCCA) were measured in early, middle, and late pregnancy and adjusted for urinary creatinine. The placental transcriptome was analyzed using RNA-Seq. Using generalized linear regression, we identified differentially expressed genes (DEGs) associated with the sum of each metabolite across pregnancy, as well as those associated with location of residence and season of birth. Pathway and upstream transcription factor analyses were performed to examine potential mechanisms associated with DEGs. Notably, TDCCA and CDCCA levels peaked in late pregnancy, with significant regional differences, particularly higher levels in the Fang region. Placental gene expression analysis showed no DEGs associated with individual metabolites at FDR<0.05. However, 251 DEGs by location, implicating immune response and oxidative phosphorylation pathways, were identified, while season of birth was associated with 2585 DEGs, over-represented in fibrosis signaling and metabolism pathways. Finally, transcription factor analysis identified 226 and 282 transcription factors associated with location and season, respectively, related to cell proliferation, differentiation, and the immune system. These alterations may have significant implications for fetal development and other pathologic processes, highlighting the importance of monitoring environmental exposures during pregnancy.

Multi-organ developmental toxicity and its characteristics in fetal mice induced by dexamethasone at different doses, stages, and courses during pregnancy.

Dexamethasone is widely used in pregnant women at risk of preterm birth to reduce the occurrence of neonatal respiratory distress syndrome and subsequently reduce neonatal mortality. Studies have suggested that dexamethasone has developmental toxicity, but there is a notable absence of systematic investigations about its characteristics. In this study, we examined the effects of prenatal dexamethasone exposure (PDE) on mother/fetal mice at different doses (0.2, 0.4, or 0.8mg/kg b.i.d), stages (gestational day 14-15 or 16-17) and courses (single- or double-course) based on the clinical practice. Results showed that PDE increased intrauterine growth retardation rate, and disordered the serum glucose, lipid and cholesterol metabolic phenotypes, and sex hormone level of mother/fetal mice. PDE was further discovered to interfere with the development of fetal lung, hippocampus and bone, inhibits steroid synthesis in adrenal and testis, and promotes steroid synthesis in the ovary and lipid synthesis in the liver, with significant effects observed at high dose, early stage and double course. The order of severity might be: ovary > lung > hippocampus/bone > others. Correlation analysis revealed that the decreased serum corticosterone and insulin-like growth factor 1 (IGF1) levels were closely related to PDE-induced low birth weight and abnormal multi-organ development in offspring. In conclusion, this study systematically confirmed PDE-induced multi-organ developmental toxicity, elucidated its characteristics, and proposed the potential "glucocorticoid (GC)-IGF1" axis programming mechanism. This research provided an experimental foundation for a comprehensive understanding of the effect and characteristics of dexamethasone on fetal multi-organ development, thereby guiding the application of "precision medicine" during pregnancy.

Association between hyperglycemia during pregnancy and offspring's refractive error: A focused review.

This review article explores the relationship between hyperglycemia during pregnancy and the visual development of offspring, specifically focusing on refractive error. The authors conducted a comprehensive search for relevant articles in various databases and assessed the methodological quality of the included studies. The findings consistently indicate that hyperglycemia during pregnancy can have a detrimental impact on the structural and functional aspects of visual development in offspring. The intrauterine hyperglycemic environment appears to negatively affect the retina and lens, leading to refractive errors. In conclusion, there is likely an association between hyperglycemia during pregnancy and the development of refractive errors in offspring.

Early statin exposure influences cardiac and skeletal development with implications for ion channel transcriptomes in zebrafish

Statins, widely prescribed for cholesterol management by inhibiting HMG-CoA reductase in the cholesterol biosynthesis pathway, may also influence vertebrate development. In this study, we investigated the developmental effects of two widely used statins, atorvastatin (ATO) and pravastatin (PRA), on zebrafish offspring. For ATO, we administered doses classified as low (1 μM), medium (5 μM), and high (10 μM), while for PRA, the corresponding concentrations were set at low (18 μM), medium (180 μM), and high (270 μM). Our results showed significant reductions in birth and hatching rates, along with decreased body length in offspring at all ATO concentrations and medium to high PRA concentrations. A notable increase in malformation rates, especially in the spine and heart, was observed across all ATO treatments and in medium and high PRA groups. Additionally, we observed reduced heart contraction rates, decreased heart size, lower bone volumes, and diminished expression of mRNA osteogenic markers. Elevated venous sinus-artery bulb (SV-BA) ratios, increased thoracic area, and abnormal cartilage development were also prominent in all ATO-treated groups. Transcriptome analysis revealed alterations in genes predominantly associated with ion channels. These findings provide insights into the potential impacts of specific concentrations of statins on offspring development and highlight potential gene interactions with statins.

Colony performance of threenative bumblebee species from South China and association with their gut microbiome.

Bumblebees play an important ecological economic role as pollinators in nature and agriculture. For reasons of biosecurity, many countries promote the cultivation of native bumblebee species for crop pollination instead of importing "alien" species. In South China, a few bumblebee species are considered useful in this way, particularly, Bombus atripes, Bombus bicoloratus and Bombus breviceps. However, whether they are suitable for artificial rearing and forming healthy colonies for pollination, remains unknown. In this project, queens from the 3 native species of Guizhou Province were collected and colonies were started under standardized conditions. The colonies were scored based on 19 parameters, including the stage of colony development, number and weight of offspring, and diet consumed. The data revealed that B.breviceps had the best performance, produced more workers and consumed the smallest diet. Next, we performed 16S rDNA sequencing of the bacterial communities found in the guts of offspring workers, and then a correlation analysis between colony performance and gut bacteria was conducted. Here, B.breviceps showed the highest diversity in gut bacterial composition, dominated by the bacteria Gilliamella, Snodgrassella, Enterobacter, and Lactobacillus Firm5. The higher the abundance of Snodgrassella, the better the performance of the colony in the foundation stage, and later Lactobacillus Firm5, Apibacter and Bifidobacterium were beneficial during the stages of rapid growth and colony decline. Although we do not understand all of the interactions yet, these correlations explain why B.breviceps demonstrated better colony performance. Our data provide valuable information for breeding local Bombus species and will contribute to developing strong colonies for crop pollination.

Activated fibroblasts modify keratinocyte stem niche through TET1 and IL-6 to promote their rapid transformation in a mouse model of prenatal arsenic exposure

Early life exposure to environmental pollutants such as arsenic (As) can increase the risk of cancers in the offspring. In an earlier study, we showed that only prenatal As exposure significantly increases epidermal stem cell proliferation and accelerates skin tumorigenesis in BALB/c mouse offspring. In the present work, we have examined the role of As-conditioned dermal fibroblasts (DFs) in creating pro-tumorigenic niches for Keratinocyte stem cells (KSCs) in the offspring. DFs isolated from prenatally exposed animals showed increased levels of activation markers (α-SMA, Fibronectin, Collagen IV), induction of ten-eleven translocation methylcytosine dioxygenase 1(TET1), and secreted high levels of niche modifying IL-6. This led to enhanced proliferation, migration, and survival of KSCs. Increased IL-6 production in As-conditioned fibroblast was driven through TET1 mediated 5-mC to 5-hmC conversion at -698/-526 and -856/-679 region on its promoter. IL-6 further acted through downstream activation of JAK2-STAT3 signaling, promoting epithelial-to-mesenchymal transition (EMT) in KSCs. Inhibition of pSTAT3 induced by IL-6 reduced the EMT process in KSCs resulting in a significant decrease in their proliferation, migration, and colony formation. Our results indicate that IL-6 produced by prenatally conditioned fibroblasts plays a major role in regulating the KSC niche and promoting skin tumor development in As-exposed offspring.

Climate-influenced performance and offspring development of merino sheep in a dry temperate-cold valley

This study aims to explore the effects of climate on the performance and offspring development of aged Merino sheep relocated from an arid, cold environment with harsh grazing conditions to a dry, temperate-cold valley with irrigated pasture production. We utilized time series data from merino sheep in a dry temperate-cold climate in southern Argentina to characterize their growth curves, assess the impact of climate on performance, and compare offspring growth with maternal growth. Our approach involved developing a dynamic model, a non-autonomous differential equation growth curve based on the widely used Brody model. The model considered variables such as local temperature, age, sex, origin, and pregnancy status to determine the optimal combination of parameters for sheep growth in our dataset. The results have shown that moving the old sheep from the steppe to the valley resulted in an increase of an average of 1 kg in weight, but their offspring had an asymptotic weight of 65 kg, 17 kg more than their mothers. The optimum temperature for the growth rate was 15.7+/-0.56 C and 8.7+/-6.3C for the asymptotic weight.

Methionine Supplementation Alleviates the Germ Cell Apoptosis Increased by Maternal Caffeine Intake in a C. elegans Model.

Caffeine (1,3,7-trimethylxanthine) is a widely consumed bioactive substance worldwide. Our recent study showed that a reduction in both reproduction and yolk protein production (vitellogenesis) caused by caffeine intake were improved by vitamin B12 supplementation, which is an essential co-factor in methionine metabolism. In the current study, we investigated the role of methionine in the reproduction of caffeine-ingested animals (CIAs). We assessed the effect of methionine metabolism on CIAs and found that caffeine intake decreased both methionine levels and essential enzymes related to the methionine cycle. Furthermore, we found that the caffeine-induced impairment of methionine metabolism decreased vitellogenesis and increased germ cell apoptosis in an LIN-35/RB-dependent manner. Interestingly, the increased germ cell apoptosis was restored to normal levels by methionine supplementation in CIAs. These results indicate that methionine supplementation plays a beneficial role in germ cell health and offspring development by regulating vitellogenesis.

Neurodevelopmental profile in children born to mothers affected by systemic sclerosis

BackgroundSystemic sclerosis (SSc) is a chronic immune-mediated connective tissue disease that can affect women of childbearing age. The long-term outcomes of their offspring remain poorly explored. Aim of this study was to detail the neurodevelopmental profile of children born to SSc mothers. MethodsTwenty children (mean age: 96 ± 4.32 months; 10 males) born to SSc mothers were enrolled. We collected data on clinical history, neurological examination, cognitive profile and adaptive behavior in all subjects. According to the chronological age, we also investigated quality of life, behavioral characteristics, psychological functioning and self-image. ResultsAll the children had normal neurological examination, cognitive profile and adaptive functioning, except for one (5 %) who suffered from Autism Spectrum Disorder. An important discrepancy was observed between parental and child opinion regarding the perception of quality of life, more compromised in the latter. We documented a risk for internalizing behavioral problems in 2 cases (10 %), for externalizing problems in 3 (15 %), for both in 1 (5 %) and for social and out-of-school activities in 5 (25 %). As regards psychological functioning, evaluated in 11 children, three (28 %) were at risk for anxiety, 1 (9 %) for depressive disorders and other 4 (36 %) for somatic disturbances. Emotional fragility and poor competence in metabolizing one's emotional experiences were observed in 9 out of the 13 subjects assessed (70 %). ConclusionsChildren born to SSc women exhibit normal cognitive and adaptive abilities but an increased vulnerability to psychopathological problems and fragility in social functioning. These observations might reflect that children need to feel mature to accept maternal chronic disease that, in turn, may hinder support for offspring's social and emotional development.

Overt hypothyroidism in pregnancy and language development in offspring: is there an association?

PurposeOvert hypothyroidism during pregnancy is linked to various obstetric complications, such as premature birth and fetal death. While some studies have shown that maternal hypothyroidism can impact a child's Intelligence Quotient (IQ) and language development, findings are controversial. The aim of this study was to explore the connection between treated maternal hypothyroidism during pregnancy and offspring neurodevelopment, focusing on learning and language and examining related maternal obstetric complications.MethodsGroup 1 included 31 hypothyroid women with elevated thyroid stimulating hormone (TSH) (> 10 mU/L, > 10 µIU/mL) during pregnancy, and Group 2 had 21 euthyroid women with normal TSH levels (0.5–2.5 mU/L, 0.5–2.5 µIU/mL). Children underwent neuropsycological assessments using the Griffiths-II scale.ResultsPregnancy outcome showed an average gestational age at delivery of 38.2 weeks for hypothyroid women, compared to 40 weeks for controls, and average birth weight of 2855.6 g versus 3285 g for controls, with hypothyroid women having children with higher intrauterine growth restriction (IUGR) prevalence and more caesarean sections. The 1-min APGAR score was lower for the hypothyroid group's children, at 8.85 versus 9.52. Neuropsychological outcomes showed children of hypothyroid mothers scored lower in neurocognitive development, particularly in the learning and language subscale (subscale C), with a notable correlation between higher maternal TSH levels and lower subscale scores.ConclusionFetuses born to hypothyroid mothers appeared to be at higher risk of IUGR and reduced APGAR score at birth. Neurocognitive development seemed to affect language performance more than the developmental quotient. This alteration appeared to correlate with the severity of hypothyroidism and its duration.

The perinatal health secondary to pandemic: association between women's delivery concerns and infant's behavioral problems.

COVID-19 pandemic characterised a unique and vulnerable social, emotional, and health environment for pregnancy, with potential long-lasting risks to maternal and child health outcomes. In women who were pregnant at the peak of COVID-19 pandemic, we investigated the association between pandemic-related concerns about pregnancy and delivery and both the parent's (i.e. maternal parenting stress) and the infant's (i.e. emotional-behavioral problems) outcomes 12 months after birth. A sample of 352 Italian pregnant women completed a web-based survey from 8 April to 4 May 2020 and a follow-up at 12 months after delivery. Maternal assessment in pregnancy covered prenatal measures for: pandemic-related concerns about pregnancy and childbirth, COVID-19 stressful events exposure, pandemic psychological stress, and mental-health symptoms (i.e. depression, anxiety). The 12 months' assessment covered post-partum measures of social support, parenting stress and maternal reports of infants' behavioral problems. The results of the Quasi-Poisson regression models on the association between COVID-19 related influencing factors and parenting stress and infant's behavioral problems showed that the presence of higher pandemic-related concerns about pregnancy and childbirth scores was associated with greater total and internalising behavioral problems but not with parenting stress levels. Perinatal mother-infant health has been sensitively threatened by pandemic consequences with maternal concerns about childbirth in pregnancy being associated with 12 months' children's behavioral outcomes. There is a need to invest in psychological support for perinatal women throughout the transition to parenthood to protect risk conditions before they get chronic or severe and influence offspring development.

Epigenetic modifications of placenta in women with gestational diabetes mellitus and their offspring.

Gestational diabetes mellitus (GDM) is a pregnancy-related complication characterized by abnormal glucose metabolism in pregnant women and has an important impact on fetal development. As a bridge between the mother and the fetus, the placenta has nutrient transport functions, endocrine functions, etc., and can regulate placental nutrient transport and fetal growth and development according to maternal metabolic status. Only by means of placental transmission can changes in maternal hyperglycemia affect the fetus. There are many reports on the placental pathophysiological changes associated with GDM, the impacts of GDM on the growth and development of offspring, and the prevalence of GDM in offspring after birth. Placental epigenetic changes in GDM are involved in the programming of fetal development and are involved in the pathogenesis of later chronic diseases. This paper summarizes the effects of changes in placental nutrient transport function and hormone secretion levels due to maternal hyperglycemia and hyperinsulinemia on the development of offspring as well as the participation of changes in placental epigenetic modifications due to maternal hyperglycemia in intrauterine fetal programming to promote a comprehensive understanding of the impacts of placental epigenetic modifications on the development of offspring from patients with GDM.

Maternal tobacco exposure during pregnancy and atopic dermatitis in offspring: A systematic review and meta-analysis.

The main purpose of this review was to examine the evidence of the relationship between active smoking or passive smoking during pregnancy and atopic dermatitis in offspring. The protocol was written following the PRISMA Checklist and was registered in the PROSPERO database (registration number CRD42022381136). We implemented a comprehensive search in PubMed, Embase and Web of Science databases to identify all potentially related articles from inception through 1 December 2022. We assessed cohort studies and case-control studies using the Newcastle-Ottawa Scale (NOS), and the Joanna Briggs Institute (JBI) critical appraisal tool to assess the quality of cross-sectional studies. Heterogeneity was investigated by using Cochrane Q tests and I2 statistics. In addition, according to the research design, population source and population size, the reasons for the heterogeneity were analysed. A total of 15 observational studies were included in this analysis. Our meta-analysis suggests that atopic dermatitis in offspring is not associated with active smoking during pregnancy (pooled OR, 0.96 [95% CI 0.86-1.07]); however, it is related to passive smoking (OR, 1.52 [95% CI 1.36-1.70]). Passive smoking during pregnancy is associated with an increased risk of eczema development in offspring. More research is needed to explore the risk of active smoking and eczema development in offspring, especially the association between measurements of pregnancy cotinine levels in maternal body fluids and AD in offspring.

Associations of parental age at pregnancy with adolescent cognitive development and emotional and behavioural problems: a birth cohort in rural Western China

BackgroundThe relationship between parental age at pregnancy and offspring development in low- and middle-income countries remains unclear. We aimed to examine the associations of parental age at pregnancy with adolescent development in rural China.MethodsWe conducted a prospective birth cohort study of offspring born to pregnant women who participated in an antenatal micronutrient supplementation trial in rural Western China. Adolescent cognitive development and emotional and behavioural problems were assessed by using the Wechsler Intelligence Scale for Children-IV and the Youth Self-Report-2001, respectively. After accounting for the possible nonlinear relationships, we examined the linear associations between parental age (in years) at pregnancy and scores of adolescent cognitive development and emotional and behavioural problems by performing generalized estimating equations.ResultsAmong 1897 adolescents followed from birth to early adolescence, 59.5% were male with a mean age of 11.8 (standard deviation (SD): 0.8) years. The mean ages of mothers and fathers at pregnancy were 24.6 (SD: 4.4) and 27.9 (SD: 4.1) years old, respectively. All the P values of the nonlinear terms between parental age and adolescent development in all domains were greater than 0.05. Each one-year increase in maternal age at pregnancy was associated with a 0.29-point (95% confidence interval (CI) 0.06, 0.52) increase in the full-scale intelligence quotient in early adolescence. After parental age was categorized into quartiles, the total behavioural problem scores of adolescents with fathers with an age in the fourth quartile (Q4) were 6.71 (95% CI 0.86, 12.57) points higher than those of adolescents with fathers with an age in the first quartile (Q1), with a linear trend P value of 0.01. Similarly, higher scores (worse behavioural problems) were observed for internalizing behavioural problems and other emotional and behavioural symptoms related to anxiety, withdrawal, social problems, thought problems and aggressive behaviour.ConclusionsAt conception, older maternal age was independently linked to better adolescent cognitive development, whereas advanced paternal age was independently associated with a greater risk of adolescent emotional and behavioral problems. These findings suggest that public health policies targeting an optimal parental age at pregnancy should be developed in the context of offspring developmental consequences.

Long-Term Effects of Maternal Fat Consumption on the Brain Transcriptome of Obesogenic Diet-Fed Young Adult Mice Offspring

BackgroundSubstantial evidence has demonstrated that maternal high-fat (HF) consumption during gestation and lactation plays as a risk factor for neurodevelopmental alterations and subsequent neurological disorders. ObjectiveWe investigated the regulatory mechanisms of maternal fat consumption on brain development and function in offspring at different ages. MethodsMouse dams were fed either a control diet [low-fat (LF)] or an HF diet for 3 wk before mating and throughout pregnancy and lactation. Offspring were killed at postnatal day (PD) 21 (LF21 and HF21), and the rest were fed an HF diet for 12 wk until the killing at PD 105 (LF105 and HF105). The expression levels of genes and proteins in the brains of offspring were analyzed by microarray and immunoblotting, respectively. ResultsMaternal dietary fat content, offspring age, and their interaction affected the expression levels of 1215, 10,453, and 2105 genes, respectively. The 67 differentially expressed genes (DEGs) between the HF21 and LF21 groups were enriched in several Gene Ontology terms related to nervous system development. Among 45 DEGs of the HF105/LF105 comparison, several genes associated with neurotransmitter action are detected. In addition, we observed increased activation of the AMP-dependent protein kinase–cAMP response element binding protein signaling pathway in HF105/LF105 comparison. However, maternal fat content did not change the protein levels of amyloid-β and tau hyperphosphorylation, the markers of neuropathogenesis. ConclusionsMaternal HF feeding altered the expression of genes involved in the development and neurotransmitter system in the brains of PD 21 and HF diet-fed PD 105 offspring, respectively. Especially, the absence of overlap between DEGs at each comparison highlights the dynamic nature of alterations in gene expression in offspring of dams fed an HF diet. Further investigation on older adult offspring is necessary to elucidate the effects of maternal fat intake on the brain pathophysiology of offspring.

Prenatal dexamethasone exposure impairs rat blood-testis barrier function and sperm quality in adult offspring via GR/KDM1B/FSTL3/TGFβ signaling.

Both epidemiological and animal studies suggest that adverse environment during pregnancy can change the offspring development programming, but it is difficult to achieve prenatal early warning. In this study we investigated the impact of prenatal dexamethasone exposure (PDE) on sperm quality and function of blood-testis barrier (BTB) in adult offspring and the underlying mechanisms. Pregnant rats were injected with dexamethasone (0.1, 0.2 and 0.4 mg·kg-1·d-1, s.c.) from GD9 to GD20. After weaning (PW4), the pups were fed with lab chow. At PW12 and PW28, the male offspring were euthanized to collect blood and testes samples. We showed that PDE significantly decreased sperm quality (including quantity and motility) in male offspring, which was associated with impaired BTB and decreased CX43/E-cadherin expression in the testis. We demonstrated that PDE induced morphological abnormalities of fetal testicle and Sertoli cell development originated from intrauterine. By tracing to fetal testicular Sertoli cells, we found that PDE dose-dependently increased expression of histone lysine demethylases (KDM1B), decreasing histone 3 lysine 9 dimethylation (H3K9me2) levels of follistatin-like-3 (FSTL3) promoter region and increased FSTL3 expression, and inhibited TGFβ signaling and CX43/E-cadherin expression in offspring before and after birth. These results were validated in TM4 Sertoli cells following dexamethasone treatment. Meanwhile, the H3K9me2 levels of FSTL3 promoter in maternal peripheral blood mononuclear cell (PBMC) and placenta were decreased and its expression increased, which was positively correlated with the changes in offspring testis. Based on analysis of human samples, we found that the H3K9me2 levels of FSTL3 promoter in maternal blood PBMC and placenta were positively correlated with fetal blood testosterone levels after prenatal dexamethasone exposure. We conclude that PDE can reduce sperm quality in adult offspring rats, which is related to the damage of testis BTB via epigenetic modification and change of FSTL3 expression in Sertoli cells. The H3K9me2 levels of the FSTL3 promoter and its expression in the maternal blood PBMC can be used as a prenatal warning marker for fetal testicular dysplasia.

Association between maternal prenatal depressive symptoms and offspring epigenetic aging at 3-5 weeks

Epigenetic clocks are emerging as tools for assessing acceleration and deceleration of biological age during childhood. Maternal depression during pregnancy may affect the biological aging of offspring and related development. In a low-income cohort of mother-child dyads, we investigated the relationship between prenatal maternal depressive symptoms and infant epigenetic age residuals, which represent the deviation (acceleration or deceleration) that exists between predicted biological age and chronological age. The epigenetic age residuals were derived from a pediatric-specific buccal epithelial clock. We hypothesized that maternal depressive symptoms, both sub-clinical and elevated (clinical level), would be associated with estimated biological age deceleration in offspring during early infancy. We analyzed data from 94 mother-child dyads using the Edinburgh Postnatal Depression Scale (EPDS) and DNA methylation derived from offspring buccal cells collected at 3–5 weeks of age. There was a significant non-linear association between the EPDS score and epigenetic age residual (β = −0.017, 95% confidence interval: −0.03,−0.01, P = <0.01). The results indicated that infants of mothers with sub-clinical depressive symptoms had the lowest infant epigenetic age residuals while infants of mothers with no-to-low depressive symptoms had the highest and experienced biological age acceleration. Maternal depressive symptoms may influence the biological aging of offspring living in poverty.

Fitness Costs of Early Life Adversity in Primates

As arguably the most critical period of mammalian development, early life can be defined as the period from conception to reproductive maturity (Tung et al., 2016). The importance of adequate nutrition and proper maternal care for maximizing the survival and development of offspring has been demonstrated through research findings in various species (Lu et al., 2018). However, these ideal growth conditions are difficult to achieve for wild offspring, who often have to overcome various energetically or socially challenging conditions that limit their development in early life. This paper will focus on the effect that environmental and social adversities have on the fitness of wild and captive non-human primates as measured by lifespan and reproductive success. Current research suggests that early life adversity in non-human primates reduces individual fitness by decreasing lifespan, fertility, and offspring survival. This paper will explore and discuss the various factors that contribute to this fitness reduction. These factors include but are not limited to: increased risk of physical illness and behavioral disorders, social isolation, maternal death, intergenerational effects, reduced female fertility, maternal stress, delayed sexual maturation, and lower adult body size.

Ocean warming shapes embryonic developmental prospects of the next generation in Atlantic cod

Abstract Although early embryonic protein production relies exclusively on maternal molecules such as messenger RNAs (mRNAs) incorporated into ovarian follicles, knowledge about any thermally induced, intergenerational effects is scarce in ectotherms. Here, we investigated how elevated temperatures (9°–12°C vs. 6°C) during oogenesis influenced the next generation by targeting maternal mRNAs in Atlantic cod (Gadus morhua) embryos, in view of up- and down-regulated genes in ovarian follicles of pre-spawning adults. Overall, the spawning female liver showed significantly higher levels of free amino acids and N-metabolites at 9°C than at 6°C. Higher-than-optimal temperatures induced adjustments in embryo transcriptome proportional to the temperature increase relative to the control group. The adjustments included alterations in maternal-effect genes, which are developmentally conserved among vertebrates. The transcriptomic differences for a selection of genes in embryos were reflected in ovarian follicles (containing multiple cell types) several months ahead of the spawning season, implying that environmental conditions of the adults are key for adjusting the genetic instructions for offspring development. This programming of fundamental traits from mother to offspring appears part of a sophisticated process to adapt the offspring to a changing ocean, though within life stage-specific, physiological thermal tolerance windows.

Maternal-driven immune education in offspring.

Maternal environmental exposures, particularly during gestation and lactation, significantly influence the immunological development and long-term immunity of offspring. Mammalian immune systems develop through crucial inputs from the environment, beginning in utero and continuing after birth. These critical developmental windows are essential for proper immune system development and, once closed, may not be reopened. This review focuses on the mechanisms by which maternal exposures, particularly to pathogens, diet, and microbiota, impact offspring immunity. Mechanisms driving maternal-offspring immune crosstalk include transfer of maternal antibodies, changes in the maternal microbiome and microbiota-derived metabolites, and transfer of immune cells and cytokines via the placenta and breastfeeding. We further discuss the role of transient maternal infections, which are common during pregnancy, in providing tissue-specific immune education to offspring. We propose a "maternal-driven immune education" hypothesis, which suggests that offspring can use maternal encounters that occur during a critical developmental window to develop optimal immune fitness against infection and inflammation.