Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1071356 | ENA |
REPOSITORIES: ENA
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Project description:Development of the gut microbiota is greatly impacted in preterm infants. Despite increasing knowledge about microbiota composition in preterm infants, knowledge about the functional signatures of the intestinal microbiota remains limited. The aim was to study transitions in microbiota activity during the first six postnatal weeks in ten preterm infants. A total of 64 stool samples were measured by LC-MS/MS.
2017-07-14 | PXD005574 | Pride
Project description:Development of the gut microbiota is greatly impacted in preterm infants. Despite increasing knowledge about microbiota composition in preterm infants, knowledge about the functional signatures of the intestinal microbiota remains limited. The aim was to study transitions in microbiota activity during the first six postnatal weeks in ten preterm infants. A total of 64 stool samples were measured by LC-MS/MS.
2017-10-17 | MSV000081616 | MassIVE
Project description:Intestinal microbiota colonization is important for intestinal development and health of preterm infants, especially those with extremely low birth weight. Recent studies indicated for a dynamic crosstalk between that gut microbiota and DNA methylome of host intestinal cells. Thereby, we sought to determine the epigenomic and metagenomic consequences of suppression of microbiota colonization in the intestine of preterm neonates to gain insights into biological pathways that shape the interface between the gut microbiota and the preterm intestinal cells. We examined 14 preterm piglets by comparing the conventional preterm neonates with those ones treated with oral antibiotics for genome wide DNA methylation and 16S rDNA microbiome. Our results demonstrated an extensive genome-wide DNA methylation changes in response to the suppression of intestinal microbe colonization, especially genes involved in neonatal immune response signaling and glycol-metabolism pathways were identified. Our study highlights several key genes that might predispose preterm neonates to NEC risk due to their key roles involved in the immune-metabolic networks. Our study not only provided rich omic-data to interpret molecular program in relation with microbiota-associated methylome-proteome network changes, but also confer clinical usage of key gene markers for potential early diagnostics of NEC of preterm neonates.
2017-10-12 | GSE88697 | GEO
Project description:Single-cell sequencing of intestinal macrophage was peformed with mice colony stimulating factor 1 receptor promoter (CSF1R) positive cells isolated from the 1/3 distal part of the small intestine of male MaFIA mice at postnatal day 17. Intestinal secretory Paneth cells become differentiated during the first two weeks after birth, which coincides with initial gut microbiota exposure. Their number is significantly reduced in cases of necrotizing enterocolitis (NEC), a deadly disease affecting premature infants. Although known to be associated with intestinal immaturity, its underlying disease mechanisms are unclear. Our analysis of mice treated with antibiotics reveals Paneth cell defects, which promote NEC pathogenesis. Our single cell and genetic analyses demonstrate that gut microbiota induces stem cell differentiation into Paneth cells by controlling the number and heterogeneity of macrophage populations that secrete Wnt ligands. Moreover, differentiated M2 macrophages are able to restore Paneth cell differentiation and rescue NEC-like pathology, while the ablation of Paneth cells is sufficient to induce it, leading to lethality. Our work reveals an unexpected requirement for Paneth cell differentiation through the regulation of gut microbiota-macrophage niches in early postnatal development.
2022-12-16 | GSE141561 | GEO
Project description:Although modern clinical practices such as cesarean sections and perinatal antibiotics have improved infant survival, treatment with broad-spectrum antibiotics alters intestinal microbiota and causes dysbiosis. Infants exposed to perinatal antibiotics have an increased likelihood of life-threatening infections, including pneumonia. Here, we investigated how the gut microbiota sculpt pulmonary immune responses, promoting recovery and resolution of infection in newborn rhesus macaques. Early-life antibiotic exposure interrupted the maturation of intestinal commensal bacteria and disrupted the developmental trajectory of the pulmonary immune system, as assessed by single-cell proteomic and transcriptomic analyses. Early-life antibiotic exposure rendered newborn macaques more susceptible to bacterial pneumonia, concurrent with increases in neutrophil senescence and hyperinflammation, broad inflammatory cytokine signaling, and macrophage dysfunction. This pathogenic reprogramming of pulmonary immunity was further reflected by a hyperinflammatory signature in all pulmonary immune cell subsets coupled with a global loss of tissue-protective, homeostatic pathways in the lungs of dysbiotic newborns. Fecal microbiota transfer was associated with partial correction of the broad immune maladaptations and protection against severe pneumonia. These data demonstrate the importance of intestinal microbiota in programming pulmonary immunity and support the idea that gut microbiota promote the balance between pathways driving tissue repair and inflammatory responses associated with clinical recovery from infection in infants. Our results highlight a potential role for microbial transfer for immune support in these at-risk infants.
2022-06-15 | GSE176408 | GEO
Project description:Altering the intestinal microbiota during a critical developmental window has lasting metabolic consequences [30_week_Liver]
2014-09-08 | E-GEOD-58086 | ExpressionAtlas
Project description:Altering the intestinal microbiota during a critical developmental window has lasting metabolic consequences [8_week_ileal]
2014-09-08 | E-GEOD-58085 | ExpressionAtlas
Project description:Maternal secretor status is one of the determinants of human milk oligosaccharides (HMOs) composition, which in turn changes the gut microbiota composition of infants. To understand if this change in gut microbiota impacts immune cell composition, intestinal morphology and gene expression, day 21-old germ-free mice were transplanted with fecal microbiota from infants whose mothers were either secretors (SMM) or non-secretors (NSM) or from infants consuming dairy-based formula (MFM). For each group, one set of mice was supplemented with HMOs. HMO supplementation did not significantly impact the microbiota diversity however, SMM mice had higher abundance of genus Bacteroides, Bifidobacterium, and Blautia, whereas, in the NSM group, there were higher abundance of Akkermansia, Enterocloster, and Klebsiella. In MFM, gut microbiota was represented mainly by Parabacteroides, Ruminococcaceae_unclassified, and Clostrodium_sensu_stricto. In mesenteric lymph node, Foxp3+ T cells and innate lymphoid cells type 2 (ILC2) were increased in MFM mice supplemented with HMOs while in the spleen, they were increased in SMM+HMOs mice. Similarly, serum immunoglobulin A (IgA) was also elevated in MFM+HMOs group. Distinct global gene expression of the gut was observed in each microbiota group, which was enhanced with HMOs supplementation. Overall, our data shows that distinct infant gut microbiota due to maternal secretor status or consumption of dairy-based formula and HMO supplementation impacts immune cell composition, antibody response and intestinal gene expression in a mouse model.
2024-03-12 | GSE260491 | GEO
Project description:Gene expression accompanying the promotion of hepatocellular carcinoma by intestinal microbiota and Tlr4 in mice.
2014-10-10 | E-GEOD-30485 | ExpressionAtlas