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Article ; Online: Effects of the in utero environment on the epigenome.

Saffery, Richard

Epigenomics

2017 Volume 9, Issue 3, Page(s) 209–211

MeSH term(s)	Animals ; Epigenesis, Genetic ; Epigenomics/methods ; Female ; Gene-Environment Interaction ; Humans ; Maternal Exposure ; Pregnancy ; Prenatal Exposure Delayed Effects/genetics
Language	English
Publishing date	2017-02-22
Publishing country	England
Document type	Editorial ; Introductory Journal Article
ISSN	1750-192X
ISSN (online)	1750-192X
DOI	10.2217/epi-2017-0017
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Article: Australian parental perceptions of genomic newborn screening for non-communicable diseases.

Casauria, Sarah / Lewis, Sharon / Lynch, Fiona / Saffery, Richard

Frontiers in genetics

2023 Volume 14, Page(s) 1209762

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2023-06-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2023.1209762
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Article: Triiodothyronine (T3) Induces Limited Transcriptional and DNA Methylation Reprogramming in Human Monocytes.

Shepherd, Rebecca / Kim, Bowon / Saffery, Richard / Novakovic, Boris

Biomedicines

2022 Volume 10, Issue 3

Abstract: Thyroid hormones have immunomodulatory roles, but their effects on the transcriptome and epigenome of innate immune cell types remain unexplored. In this study, we investigate the effects of triiodothyronine (T3) on the transcriptome and methylome of ... ...

Abstract	Thyroid hormones have immunomodulatory roles, but their effects on the transcriptome and epigenome of innate immune cell types remain unexplored. In this study, we investigate the effects of triiodothyronine (T3) on the transcriptome and methylome of human monocytes in vitro, both in resting and lipopolysaccharide (LPS)-stimulated conditions. In resting monocytes, 5 µM T3 affected the expression of a small number of monocyte-to-macrophage differentiation-associated genes, including TLR4 (p-value < 0.05, expression fold change >1.5). T3 attenuated a small proportion of monocyte-to-macrophage differentiation-associated DNA methylation changes, while specifically inducing DNA methylation changes at several hundred differentially methylated CpG probes (DMPs) (p-value < 0.05, Δβ > 0.05). In LPS-stimulated monocytes, the presence of T3 attenuated the effect of 27% of LPS-induced DMPs (p-value < 0.05, Δβ > 0.05). Interestingly, co-stimulation with T3 + LPS induced a unique DNA methylation signature that was not observed in the LPS-only or T3-only exposure groups. Our results suggest that T3 induces limited transcriptional and DNA methylation remodeling in genes enriched in metabolism and immune processes and alters the normal in vitro LPS response. The overlap between differentially expressed genes and genes associated with DMPs was minimal; thus, other epigenetic mechanisms may underpin the expression changes. This research provides insight into the complex interplay between thyroid hormones, epigenetic remodeling, and transcriptional dynamics in monocytes.
Language	English
Publishing date	2022-03-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines10030608
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Article ; Online: Epigenetic change as the major mediator of fetal programming in humans: Are we there yet?

Saffery, Richard

Annals of nutrition & metabolism

2014 Volume 64, Issue 3-4, Page(s) 203–207

Abstract: The developmental origins of health and disease (DOHaD) hypothesis predicts that environmental exposures experienced early in life have the potential to modify the risk associated with later-onset disease. The DOHaD hypothesis is supported by a large ... ...

Abstract	The developmental origins of health and disease (DOHaD) hypothesis predicts that environmental exposures experienced early in life have the potential to modify the risk associated with later-onset disease. The DOHaD hypothesis is supported by a large number of direct animal studies and a smaller number of compelling observational studies in humans, but the mechanism(s) underlying the 'programming' effects of DOHaD remain largely unclear. Given the inherent property of environmental sensitivity, the demonstrated role in gene regulation, and the capacity for stable maintenance over time once established, epigenetic variation has rapidly emerged as a candidate mediator of such effects. However, little direct evidence exists in humans, primarily due to the inherent problems associated with unraveling the relative contributions of genetic and environmental influences to phenotypic outcomes. Robust evidence is required in several domains to establish epigenetic variation in the causal pathway to DoHAD-associated disease. Firstly, interindividual epigenetic variability in response to specific early-life environmental exposures needs to be demonstrated. Further, compelling data linking specific epigenetic variants to specific disease(s) is needed. Epigenetic variation should be apparent in a tissue relevant to the disease of interest prior to phenotypic onset in order to avoid confounding and the potential for reverse causation. Finally, the functional relevance of specific epigenetic change must be demonstrated. Compelling evidence is mounting in each of these domains but remains somewhat fragmented, providing small pieces of the overall complex puzzle. It is likely that only large longitudinal life course studies commencing prior to birth, with extensive environmental exposure data and biospecimens, can provide direct evidence in support of a role of epigenetic processes as drivers of the DOHaD in humans.
MeSH term(s)	Aging ; Epigenesis, Genetic ; Female ; Fetal Development ; Health Status ; Humans ; Male ; Models, Biological ; Precision Medicine/trends ; Pregnancy
Language	English
Publishing date	2014
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	392341-1
ISSN	1421-9697 ; 0250-6807 ; 1018-9688
ISSN (online)	1421-9697
ISSN	0250-6807 ; 1018-9688
DOI	10.1159/000365020
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Article ; Online: Association of Polygenic Risk Scores for Hearing Difficulty in Older Adults With Hearing Loss in Mid-Childhood and Midlife: A Population-Based Cross-sectional Study Within the Longitudinal Study of Australian Children.

Wang, Jing / Lange, Katherine / Sung, Valerie / Morgan, Angela / Saffery, Richard / Wake, Melissa

JAMA otolaryngology-- head & neck surgery

2023 Volume 149, Issue 3, Page(s) 204–211

Abstract: Importance: Although more than 200 genes have been associated with monogenic congenital hearing loss, the polygenic contribution to hearing decline across the life course remains largely unknown.: Objective: To examine the association of polygenic ... ...

Abstract	Importance: Although more than 200 genes have been associated with monogenic congenital hearing loss, the polygenic contribution to hearing decline across the life course remains largely unknown. Objective: To examine the association of polygenic risk scores (PRSs) for self-reported hearing difficulty among adults (40-69 years) with measured hearing and speech reception abilities in mid-childhood and early midlife. Design, setting, and participants: This was a population-based cross-sectional study nested within the Longitudinal Study of Australian Children that included 1608 children and 1642 adults. Pure tone audiometry, speech reception threshold against noise, and genetic data were evaluated. Linear and logistic regressions of PRSs were conducted for hearing outcomes. Study analysis was performed from March 1 to 31, 2022. Main outcomes and measures: Genotypes were generated from saliva or blood using global single-nucleotide polymorphisms array and PRSs derived from published genome-wide association studies of self-reported hearing difficulty (PRS1) and hearing aid use (PRS2). Hearing outcomes were continuous using the high Fletcher index (mean hearing threshold, 1, 2, and 4 kHz) and speech reception threshold (SRT); and dichotomized for bilateral hearing loss of more than 15 dB HL and abnormal SRT. Results: Included in the study were 1608 children (mean [SD] age, 11.5 [0.5] years; 812 [50.5%] male children; 1365 [84.9%] European and 243[15.1%] non-European) and 1642 adults (mean [SD] age, 43.7 [5.1] years; 1442 [87.8%] female adults; 1430 [87.1%] European and 212 [12.9%] non-European individuals). In adults, both PRS1 and PRS2 were associated with hearing thresholds. For each SD increment in PRS1 and PRS2, hearing thresholds were 0.4 (95% CI, 0-0.8) decibel hearing level (dB HL) and 0.9 (95% CI, 0.5-1.2) dB HL higher on the high Fletcher index, respectively. Each SD increment in PRS increased the odds of adult hearing loss of more than 15 dB HL by 10% to 30% (OR for PRS1, 1.1; 95% CI, 1.0-1.3; OR for PRS2, 1.3; 95% CI, 1.1-1.5). Similar but attenuated patterns were noted in children (OR for PRS1, 1.1; 95% CI, 0.8-1.2; OR for PRS2, 1.2; 95% CI, 1.0-1.5). Both PRSs showed minimal evidence of associations with speech reception thresholds or abnormal SRT in children or adults. Conclusions and relevance: This population-based cross-sectional study of PRSs for self-reported hearing difficulty among adults found an association with hearing ability in mid-childhood. This adds to the evidence that age-related hearing loss begins as early as the first decade of life and that polygenic inheritance may play a role together with other environmental risk factors.
MeSH term(s)	Child ; Humans ; Male ; Female ; Aged ; Adult ; Longitudinal Studies ; Cross-Sectional Studies ; Genome-Wide Association Study ; Multifactorial Inheritance ; Australia ; Hearing ; Deafness ; Risk Factors ; Presbycusis ; Audiometry, Pure-Tone
Language	English
Publishing date	2023-01-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701825-8
ISSN	2168-619X ; 2168-6181
ISSN (online)	2168-619X
ISSN	2168-6181
DOI	10.1001/jamaoto.2022.4466
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Article ; Online: Clarifying the Sweeping Consequences of COVID-19 in Pregnant Women, Newborns, and Children With Existing Cohorts.

Hu, Yanhong Jessika / Wake, Melissa / Saffery, Richard

JAMA pediatrics

2020 Volume 175, Issue 2, Page(s) 117–118

MeSH term(s)	Adult ; COVID-19/epidemiology ; COVID-19/physiopathology ; Child ; Female ; Humans ; Infant Welfare/statistics & numerical data ; Infant, Newborn ; Infectious Disease Transmission, Vertical/prevention & control ; Infectious Disease Transmission, Vertical/statistics & numerical data ; Maternal Welfare/statistics & numerical data ; Pregnancy ; Pregnancy Complications, Infectious/epidemiology ; Pregnancy Complications, Infectious/prevention & control
Keywords	covid19
Language	English
Publishing date	2020-08-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	2701223-2
ISSN	2168-6211 ; 2168-6203
ISSN (online)	2168-6211
ISSN	2168-6203
DOI	10.1001/jamapediatrics.2020.2395
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Article ; Online: Mapping Pulmonary and Systemic Inflammation in Preschool Aged Children With Cystic Fibrosis.

Shanthikumar, Shivanthan / Ranganathan, Sarath C / Saffery, Richard / Neeland, Melanie R

Frontiers in immunology

2021 Volume 12, Page(s) 733217

Abstract: The immune landscape of the paediatric respiratory system remains largely uncharacterised and as a result, the mechanisms of globally important childhood respiratory diseases remain poorly understood. In this work, we used high parameter flow cytometry ... ...

Abstract	The immune landscape of the paediatric respiratory system remains largely uncharacterised and as a result, the mechanisms of globally important childhood respiratory diseases remain poorly understood. In this work, we used high parameter flow cytometry and inflammatory cytokine profiling to map the local [bronchoalveolar lavage (BAL)] and systemic (whole blood) immune response in preschool aged children with cystic fibrosis (CF) and aged-matched healthy controls. We demonstrate that children with CF show pulmonary infiltration of CD66b
MeSH term(s)	Biomarkers/blood ; Bronchoalveolar Lavage Fluid/immunology ; Case-Control Studies ; Cystic Fibrosis/diagnosis ; Cystic Fibrosis/immunology ; Cystic Fibrosis/metabolism ; Cytokines/blood ; Flow Cytometry ; Humans ; Immunophenotyping ; Inflammation/diagnosis ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation Mediators/blood ; Leukocytes/immunology ; Leukocytes/metabolism ; Phenotype ; Pneumonia/diagnosis ; Pneumonia/immunology ; Pneumonia/metabolism
Chemical Substances	Biomarkers ; Cytokines ; Inflammation Mediators
Language	English
Publishing date	2021-10-15
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.733217
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Article: Blood Plasma Metabolites in Diabetes-Associated Chronic Kidney Disease: A Focus on Lipid Profiles and Cardiovascular Risk.

Lecamwasam, Ashani / Mansell, Toby / Ekinci, Elif I / Saffery, Richard / Dwyer, Karen M

Frontiers in nutrition

2022 Volume 9, Page(s) 821209

Abstract: Background: We investigated a cross-sectional metabolomic analysis of plasma and urine of patients with early and late stage diabetes associated chronic kidney disease (CKD), inclusive of stages 1-5 CKD, to identify potential metabolomic profiles ... ...

Abstract	Background: We investigated a cross-sectional metabolomic analysis of plasma and urine of patients with early and late stage diabetes associated chronic kidney disease (CKD), inclusive of stages 1-5 CKD, to identify potential metabolomic profiles between the two groups. Methods: This cross-sectional study recruited 119 adults. Metabolomic biomarkers were quantified in 119 non-fasted plasma and 57 urine samples using a high-throughput proton Nuclear Magnetic Resonance platform. Analyses were conducted using R with the ggforestplot package. Linear regression models were minimally adjusted for age, sex, and body mass index and Results: Apolipoprotein A1 concentration (ApoA1) was reduced (adj. Conclusion: Our results highlight the presence of abnormal lipid metabolism namely significant reduction in the protective ApoA1 and significant increase in atherogenic ApoB/ApoA1 ratio. The study also demonstrates significantly elevated levels of triglyceride-rich lipoproteins such as LDL-TG. We illustrate the significant reduction in protective HDL-C in individuals with diabetic CKD. It explores a detailed plasma lipid profile that significantly differentiates between the late and early CKD groups as well as each CKD stage. The study of complex metabolite profiles may provide additional data required to enable more specific cardiovascular risk stratification.
Language	English
Publishing date	2022-02-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2776676-7
ISSN	2296-861X
ISSN	2296-861X
DOI	10.3389/fnut.2022.821209
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Article ; Online: Effect of an antenatal diet and lifestyle intervention and maternal BMI on cord blood DNA methylation in infants of overweight and obese women: The LIMIT Randomised Controlled Trial.

Louise, Jennie / Deussen, Andrea R / Koletzko, Berthold / Owens, Julie / Saffery, Richard / Dodd, Jodie M

PloS one

2022 Volume 17, Issue 6, Page(s) e0269723

Abstract: Background: To investigate the effect of an antenatal diet and lifestyle intervention, and maternal pre-pregnancy overweight or obesity, on infant cord blood DNA methylation.: Methods: We measured DNA methylation in 645 cord blood samples from ... ...

Abstract	Background: To investigate the effect of an antenatal diet and lifestyle intervention, and maternal pre-pregnancy overweight or obesity, on infant cord blood DNA methylation. Methods: We measured DNA methylation in 645 cord blood samples from participants in the LIMIT study (an antenatal diet and lifestyle intervention for women with early pregnancy BMI ≥25.0 kg/m2) using the Illumina 450K BeadChip array, and tested for any differential methylation related to the intervention, and to maternal early pregnancy BMI. We also analysed differential methylation in relation to selected candidate genes. Results: No CpG sites were significantly differentially methylated in relation to either the diet and lifestyle intervention, or with maternal early pregnancy BMI. There was no significant differential methylation in any of the selected genes related to the intervention, or to maternal BMI. Conclusion: We found no evidence of an effect of either antenatal diet and lifestyle, or of maternal early pregnancy BMI, on cord blood DNA methylation. Clinical trials registration: ACTRN12607000161426.
MeSH term(s)	Body Mass Index ; DNA Methylation ; Diet ; Female ; Fetal Blood ; Humans ; Infant ; Life Style ; Obesity/genetics ; Obesity/therapy ; Overweight/genetics ; Overweight/therapy ; Pregnancy ; Pregnancy Complications ; Prenatal Care
Language	English
Publishing date	2022-06-24
Publishing country	United States
Document type	Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0269723
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Article ; Online: Placental DNA methylation in pregnancies complicated by maternal diabetes and/or obesity: State of the art and research gaps.

Hjort, Line / Novakovic, Boris / Cvitic, Silvija / Saffery, Richard / Damm, Peter / Desoye, Gernot

Epigenetics

2022 Volume 17, Issue 13, Page(s) 2188–2208

Abstract: SUMMARYMaternal diabetes and/or obesity in pregnancy are undoubtedly associated with later disease-risk in the offspring. The placenta, interposed between the mother and the foetus, is a potential mediator of this risk through epigenetic mechanisms, ... ...

Abstract	SUMMARYMaternal diabetes and/or obesity in pregnancy are undoubtedly associated with later disease-risk in the offspring. The placenta, interposed between the mother and the foetus, is a potential mediator of this risk through epigenetic mechanisms, including DNA methylation. In recent years, multiple studies have identified differentially methylated CpG sites in the placental tissue DNA in pregnancies complicated by diabetes and obesity. We reviewed all published original research relevant to this topic and analysed our findings with the focus of identifying overlaps, contradictions, and gaps. Most studies focused on the association of gestational diabetes and/or hyperglycaemia in pregnancy and DNA methylation in placental tissue at term. We identified overlaps in results related to specific candidate genes, but also observed a large research gap of pregnancies affected by type 1 diabetes. Other unanswered questions relate to analysis of specific placental cell types and the timing of DNA methylation change in response to diabetes and obesity during pregnancy. Maternal metabolism is altered already in the first trimester involving structural and functional changes in the placenta, but studies into its effects on placental DNA methylation during this period are lacking and urgently needed. Foetal sex is also an important determinant of pregnancy outcome, but only few studies have taken this into account. Collectively, we provide a reference work for researchers working in this large and evolving field. Based on the results of the literature review, we formulate suggestions for future focus of placental DNA methylation studies in pregnancies complicated by diabetes and obesity.
MeSH term(s)	Pregnancy ; Female ; Humans ; Diabetes, Gestational/genetics ; Diabetes, Gestational/metabolism ; DNA Methylation ; Placenta/metabolism ; Sex Factors ; Obesity/complications ; Obesity/genetics ; Obesity/metabolism ; Pregnancy Outcome/genetics
Language	English
Publishing date	2022-09-05
Publishing country	United States
Document type	Review ; Journal Article
ISSN	1559-2308
ISSN (online)	1559-2308
DOI	10.1080/15592294.2022.2111755
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