Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1000236 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25466200_1.fastq.gz | Fastqsanger.gz | |||
| SRR25466200_2.fastq.gz | Fastqsanger.gz | |||
| SRR25466300_1.fastq.gz | Fastqsanger.gz | |||
| SRR25466300_2.fastq.gz | Fastqsanger.gz | |||
| SRR25466400_1.fastq.gz | Fastqsanger.gz |
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Project description:Breastfeeding has been associated with long lasting health benefits. Nutrients and bioactive components of human breast milk promote cell growth, immune development, and shield the infant gut from insults and microbial threats. The molecular and cellular events involved in these processes are ill defined. We have established human pediatric enteroids and interrogated maternal milk’s impact on epithelial cell maturation and function in comparison with commercial infant formula. Colostrum applied apically to pediatric enteroid monolayers reduced ion permeability, stimulated epithelial cell differentiation, and enhanced tight junction function by upregulating occludin amount. Breast milk heightened the production of antimicrobial peptide -defensin 5 by goblet and Paneth cells, and modulated cytokine production, which abolished apical release of pro-inflammatory GM-CSF. These attributes were not found in commercial infant formula. Epithelial cells exposed to breast milk elevated apical and intracellular pIgR amount and enabled maternal IgA translocation. Proteomic data revealed a breast milk-induced molecular pattern associated with tissue remodeling and homeostasis. Using a novel ex vivo pediatric enteroid model, we have identified cellular and molecular pathways involved in human milk-mediated improvement of human intestinal physiology and immunity.
2022-02-17 | PXD025966 | Pride
Project description:Breastfeeding is vital for reducing morbidity and mortality, yet exclusive breastfeeding rates are low, with insufficient milk supply being a major weaning factor whose molecular causes remain largely unknown. In this study, we collected fresh milk samples from 30 lactating individuals, classified as low, normal, or high milk producers at multiple postpartum stages, and conducted extensive genomic and microbiome analysis. Using bulk RNA sequencing on human milk fat globules (MFG), milk cells, and breast tissue, we found that MFG-derived RNA closely resembles RNA from milk luminal cells. Furthermore, bulk and single-cell RNA-seq revealed changes in the transcriptome and cellular content linked to milk production. We identified specific genes and cell-type proportions differing in low and high milk production. Infant microbiome diversity was affected by feeding type, but not by maternal milk supply. This study provides a comprehensive human milk transcriptomic catalog, identifies genes associated with milk production, and highlights MFG as a useful biomarker for milk transcriptome analysis.
2024-11-30 | GSE275627 | GEO
Project description:Breastfeeding is vital for reducing morbidity and mortality, yet exclusive breastfeeding rates are low, with insufficient milk supply being a major weaning factor whose molecular causes remain largely unknown. In this study, we collected fresh milk samples from 30 lactating individuals, classified as low, normal, or high milk producers at multiple postpartum stages, and conducted extensive genomic and microbiome analysis. Using bulk RNA sequencing on human milk fat globules (MFG), milk cells, and breast tissue, we found that MFG-derived RNA closely resembles RNA from milk luminal cells. Furthermore, bulk and single-cell RNA-seq revealed changes in the transcriptome and cellular content linked to milk production. We identified specific genes and cell-type proportions differing in low and high milk production. Infant microbiome diversity was affected by feeding type, but not by maternal milk supply. This study provides a comprehensive human milk transcriptomic catalog, identifies genes associated with milk production, and highlights MFG as a useful biomarker for milk transcriptome analysis.
2024-11-30 | GSE275626 | GEO
Project description:The breast milk plays a crucial role in shaping the initial intestinal microbiota and mucosal immunity of the infant. Interestingly, breastfeeding has proven to be protective against the early onset of immune-mediated diseases including type 1 diabetes (T1D). Studies have shown that exosomes from human breast milk (HM) are enriched in immune-modulating miRNAs suggesting that exosomal miRNAs transferred to the infant could play a critical role in the development of the infant’s immune system. In this study, we extracted exosome exosomal microRNAs (exomiRs) from breast milk of type 1 diabetic and healthy lactating mothers, in order to identify any differences in the exomiR content between the two groups
2019-08-01 | E-MTAB-7336 | biostudies-arrayexpress
Project description:Human breast milk contains a diverse community of bacteria but factors that produce variation in the breast milk microbiome are largely unknown. We evaluated if 1) maternal factors including breastfeeding practices modified the diversity and abundance of bacterial communities in breast milk and 2) if subclinical mastitis (SCM), an asymptomatic inflammatory condition occurring during lactation, induced a distinctive microbiota signature.
| EGAS00001003044 | EGA
Project description:Maintenance of intestinal homeostasis requires a healthy relationship between the commensal gut microbiota and the host immune system. Breast milk supplies the first source of antigen-specific immune protection in the gastrointestinal tract of suckling mammals, in the form of secretory immunoglobulin A (SIgA). SIgA is transported across glandular and mucosal epithelial cells into external secretions by the polymeric immunoglobulin receptor (pIgR). Here, a breeding scheme with pIgR-sufficient and -deficient mice was used to study the effects of breast milk-derived SIgA on development of the gut microbiota and host intestinal immunity. Early exposure to maternal SIgA prevented the translocation of aerobic bacteria from the neonatal gut into draining lymph nodes, including the opportunistic pathogen Ochrobactrum anthropi. By the age of weaning, mice that received maternal SIgA in breast milk had a significantly different gut microbiota from mice that did not receive SIgA, and these differences were magnified when the mice reached adulthood. Early exposure to SIgA in breast milk resulted in a pattern of intestinal epithelial cell gene expression in adult mice that differed from that of mice that were not exposed to passive SIgA, including genes associated with intestinal inflammatory diseases in humans. Maternal SIgA was also found to ameliorate colonic damage caused by the epithelial-disrupting agent dextran sulfate sodium. These findings reveal unique mechanisms through which SIgA in breast milk may promote lifelong intestinal homeostasis, and provide additional evidence for the benefits of breastfeeding. We used microarrays to determine the effects of passive and active secretory IgA, in the presence or absence of the epithelial-disrupting agent dextran sulfate sodium, on gene expression in intestinal epithelial cells of mice
2014-01-25 | GSE54371 | GEO
Project description:Pediatric obesity has more than doubled in children and tripled in adolescents over the past 30 years. Recent findings demonstrate that differences in energy harvesting bacteria promote obesity in the host and appear to be influenced by early life factors such as mode of delivery, maternal obesity, and breastfeeding. The goal of this proposal is to investigate how human milk impacts the infant gut microbiome during the first 12-months of life and identify the microbe-host interactions that mediates the protective role of breastfeeding on infant adiposity. The results of this exploratory study will characterize factors that influence microbial transmission between mothers and offspring and identify human milk compounds that stabilize a healthy infant microbiome with potential to reduce pediatric obesity.
2018-04-15 | ST000957 | MetabolomicsWorkbench
Project description:Background - Prepregnancy overweight and obesity promote deleterious health impacts on both mothers during pregnancy and the offspring. Significant changes in the maternal peripheral blood mononuclear cells (PBMCs) gene expression due to obesity are well-known. However, during pregnancy the impact of overweight on immune cell gene expression and its association with maternal and infant outcomes is not well explored. Methods – Blood samples were collected from healthy normal weight (NW, BMI 18.5-24.9) or overweight (OW, BMI 25-29.9) 2nd parity pregnant women at 12, 24 and 36 weeks of pregnancy. PBMCs were isolated from the blood and subjected to mRNA sequencing. Maternal and infant microbiota were analyzed by 16S rRNA gene sequencing. Integrative multi-omics data analysis was performed to evaluate the association of gene expression with maternal diet, gut microbiota, milk composition, and infant gut microbiota. Results - Gene expression analysis revealed that 453 genes were differentially expressed in the OW women compared to NW women at 12 weeks of pregnancy, out of which 354 were upregulated and 99 were downregulated. Several up-regulated genes in the OW group were enriched in inflammatory, chemokine-mediated signaling and regulation of interleukin-8 production-related pathways. At 36 weeks of pregnancy healthy eating index score was positively associated with several genes that include, DTD1, ELOC, GALNT8, ITGA6-AS1, KRT17P2, NPW, POT1-AS1 and RPL26. In addition, at 36 weeks of pregnancy, genes involved in adipocyte functions, such as NG2 and SMTNL1, were negatively correlated to human milk 2’FL and total fucosylated oligosaccharides content collected at 1 month postnatally. Furthermore, infant Akkermansia was positively associated with maternal PBMC anti-inflammatory genes that include CPS1 and RAB7B, at 12 and 36 weeks of pregnancy. Conclusions – These findings suggest that prepregnancy overweight impacts the immune cell gene expression profile, particularly at 12 weeks of pregnancy. Further, deciphering the complex association of PBMC’s gene expression levels with maternal gut microbiome and milk composition and infant gut microbiome may aid in developing strategies to mitigate obesity-mediated effects.
2024-08-27 | GSE273780 | GEO
Project description:Maintenance of intestinal homeostasis requires a healthy relationship between the commensal gut microbiota and the host immune system. Breast milk supplies the first source of antigen-specific immune protection in the gastrointestinal tract of suckling mammals, in the form of secretory immunoglobulin A (SIgA). SIgA is transported across glandular and mucosal epithelial cells into external secretions by the polymeric immunoglobulin receptor (pIgR). Here, a breeding scheme with pIgR-sufficient and -deficient mice was used to study the effects of breast milk-derived SIgA on development of the gut microbiota and host intestinal immunity. Early exposure to maternal SIgA prevented the translocation of aerobic bacteria from the neonatal gut into draining lymph nodes, including the opportunistic pathogen Ochrobactrum anthropi. By the age of weaning, mice that received maternal SIgA in breast milk had a significantly different gut microbiota from mice that did not receive SIgA, and these differences were magnified when the mice reached adulthood. Early exposure to SIgA in breast milk resulted in a pattern of intestinal epithelial cell gene expression in adult mice that differed from that of mice that were not exposed to passive SIgA, including genes associated with intestinal inflammatory diseases in humans. Maternal SIgA was also found to ameliorate colonic damage caused by the epithelial-disrupting agent dextran sulfate sodium. These findings reveal unique mechanisms through which SIgA in breast milk may promote lifelong intestinal homeostasis, and provide additional evidence for the benefits of breastfeeding. We used microarrays to determine the effects of passive and active secretory IgA, in the presence or absence of the epithelial-disrupting agent dextran sulfate sodium, on gene expression in intestinal epithelial cells of mice A breeding scheme was used that involved crosses between mouse dams and sires that were deficient or sufficient for expression of the polymeric immunoglobulin receptor (Pigr), a protein that is required for transport of secretory IgA (SIgA) into external secretions. Offspring of these crosses were genotyped for Pigr alleles, and littermate offspring were distributed into 4 groups based on early exposure to passive SIgA in mother's milk (P-yes and P-no) and ability to carry out Pigr-mediated endogenous transport of active SIgA (A-yes and A-no). Seventy-day-old gender-matched Pigr+/- and Pigr-/- offspring of Pigr+/- and Pigr-/- dams were left untreated or given 2% dextran sulfate sodium (DSS) in drinking water for 8 days. Colonic epithelial cells were isolated, and total cellular RNA was purified. RNA was pooled from 3 mice for each of 2 biological replicates for microarray analysis.
2014-01-25 | E-GEOD-54371 | biostudies-arrayexpress
Project description:Microbiota assembly in the infant gut is influenced by time and duration of dietary exposure to breast-milk, infant formula and solid foods.
2023-10-18 | MSV000093140 | MassIVE