Effect of gut microbiome transplant from neonates of particle-exposed mothers on the epigenome of dendritic cells
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PROVIDER: PRJNA1038745 | ENA |
REPOSITORIES: ENA
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Project description:In our model the newborns of asthmatic mother mice or of mothers exposed to air pollutant particles are born with a predisposition to asthma. Gut microbiome of these pups is altered, and the transplant of the pups’ microbiome (GMT) has conferred the asthma predisposition to naïve recipients. We hypothesized that bacteria alter metabolomic profile in the gut, which polarizes the dendritic cells (DC) in the recipient by affecting epigenetic regulation in these key decision-maker cells. Here we examined DNA methylation profiles in the recipient host’s DCs to test the prediction that GMT confers alterations in DNA methylation (not seen with sterilized GMT).
2024-04-01 | GSE247470 | GEO
Project description:We report comparative transcriptome data of CD34+ cells derived from umbilical cord blood of neonates delivered from SARS-CoV-2 infected and/or vaccinated mothers or uninfected/non-vaccinated mothers.
2022-11-23 | GSE196802 | GEO
Project description:This study aims to demonstrate the link between epigenome-wide methylation aberrations at birth and genomic transcriptional changes upon allergen sensitization that occur in the neonatal dendritic cells (DC) due to maternal asthma. In an in vivo model reproducing human epidemiology findings, maternal but not paternal asthma predisposes the neonate to increased asthma risk, the effect is allergen-independent and is not genetic or environmental. Earlier we demonstrated that neonates of asthmatic mothers are born with a functional skew in splenic DCs that mediates the early-life asthma origin. These allergen-naive cells convey allergy responses to normal recipients, however minimal to no transcriptional or phenotypic changes were found to explain the functional pro-allergic alterations. In this study we profiled both allergen-naïve dendritic cells, and cells after allergen sensitization in vivo. We found that while allergen-naive DCs from asthma-at-risk neonates have minimal transcriptional change compared to controls, upon allergen sensitization, multiple genes with pre-existing epigenetic alterations show significant transcriptional change. . 24 samples from 2 batches, 3-4 replicates in each of 4 groups
2013-06-01 | E-GEOD-44678 | biostudies-arrayexpress
Project description:This study aims to demonstrate the link between epigenome-wide methylation aberrations at birth and genomic transcriptional changes upon allergen sensitization that occur in the neonatal dendritic cells (DC) due to maternal asthma. In an in vivo model reproducing human epidemiology findings, maternal but not paternal asthma predisposes the neonate to increased asthma risk, the effect is allergen-independent and is not genetic or environmental. Earlier we demonstrated that neonates of asthmatic mothers are born with a functional skew in splenic DCs that mediates the early-life asthma origin. These allergen-naive cells convey allergy responses to normal recipients, however minimal to no transcriptional or phenotypic changes were found to explain the functional pro-allergic alterations. In this study we profiled both allergen-naïve dendritic cells, and cells after allergen sensitization in vivo. We found that while allergen-naive DCs from asthma-at-risk neonates have minimal transcriptional change compared to controls, upon allergen sensitization, multiple genes with pre-existing epigenetic alterations show significant transcriptional change. .
2013-06-01 | GSE44678 | GEO
Project description:We performed reduced-representation bisulfite sequencing (RRBS) on 137 umbilical cord blood (UCB) samples and 158 parental peripheral blood (PPB) samples from nuclear families with either singletons or twins. The samples were classified into five groups based on the mode of conception: spontaneous (CTRL), IVF-ET, IVF-FET, ICSI-ET and ICSI-FET. There were no significant differences in the clinical features of the neonates among the different groups; in addition, maternal ages were under 35 years old and parental body mass index (BMI) values were comparable in general. In addition, we performed chromatin immunoprecipitation sequencing (ChIP-seq) on 33 UCB samples to examine histone modifications (H3K4me1, H3K4me3, H3K27ac, and H3K27me3) and RNA sequencing (RNA-seq) on 32 UCB samples to examine the transcriptomes of neonates.
2020-08-09 | GSE136849 | GEO
Project description:RATIONALE: In a mouse model of maternal transmission of asthma risk (J. Immunol 170:1683, 2003), baby mice of asthmatic (As), but not normal (Nrm), mothers show increased susceptibility to allergy. We previously showed that adoptive transfer to normal baby mice of dendritic cells (DCs) harvested from asthma-susceptible but allergen-naïve neonates reproduces the increased susceptibility to asthma. Hence, the maternal effect is mediated by altered neonatal DCs, which skew immune responses towards a pro-allergic Th2 phenotype. To identify potential molecular mechanisms, we performed epigenomic profiling of isolated neonatal DCs. METHODS: BALB/c mice were sensitized by 2 i.p. injections of ovalbumin (OVA) in alum and repeatedly challenged with OVA aerosols (As) prior to mating with normal males. Purified splenic CD11c+ DCs of 14-day old allergen-naïve offspring from these As and control Nrm mothers were isolated using magnetic beads. Methylation profiles of genomic DNA were obtained using Switchgear epigenomic chip arrays. After normalization and background correction analysis using significance analysis for microarrays (SAM) and ANOVA was performed. RESULTS: We identified 300 to 6000 (depending on stringency) chromosomal regions with significantly different methylation status, (2 â 10 fold). Clustering methods and pathway analysis identified several interrelated gene groups that merit further study. CONCLUSION: Maternal asthma causes multiple significant epigenetic changes in neonatal dendritic cells. Keywords: Dendritic cells, genomic DNA, DNA methylation, allergy, asthma The analysis includes 9 samples of genomic DNA from isolated splenic CD11c+ dendritic cells (>95% pure) per group. The two groups are neonates born to mothers with induced allergy to ovalbumin, and normal control neonates. All neonates are genetically and environmentally identical, and allergen-naive.
2010-06-24 | E-GEOD-13380 | biostudies-arrayexpress
Project description:<p>Maternal seeding of the microbiome in neonates promotes a long-lasting biological footprint, but how it impacts disease susceptibility in early life remains unknown. We hypothesized that feeding butyrate to pregnant mice influences the newborn’s susceptibility to biliary atresia, a severe cholangiopathy of neonates. Here, we show that butyrate administration to mothers renders newborn mice resistant to inflammation and injury of bile ducts and improves survival. The prevention of hepatic immune cell activation and survival trait is linked to fecal signatures of Bacteroidetes and Clostridia and increases glutamate/glutamine and hypoxanthine in stool metabolites of newborn mice. In human neonates with biliary atresia, the fecal microbiome signature of these bacteria is under-represented, with suppression of glutamate/glutamine and increased hypoxanthine pathways. The direct administration of butyrate or glutamine to newborn mice attenuates the disease phenotype, but only glutamine renders bile duct epithelial cells resistant to cytotoxicity by natural killer cells. Thus, maternal intake of butyrate influences the fecal microbial population and metabolites in newborn mice and the phenotypic expression of experimental biliary atresia, with glutamine promoting survival of bile duct epithelial cells.</p>
2022-01-11 | MTBLS2171 | MetaboLights
Project description:Transcriptome analysis of umbilical cord blood CD34+ cells of neonates delivered from SARS-CoV-2 infected and/or vaccinated mothers
| PRJNA807340 | ENA