Project description:We have previously demonstrated that the gut microbiota can play a role in the pathogenesis of conditions associated with exposure to environmental pollutants. It is well accepted that diets high in fermentable fibers such as inulin can beneficially modulate the gut microbiota and lessen the severity of pro-inflammatory diseases. Therefore, we aimed to test the hypothesis that hyperlipidemic mice fed a diet enriched with inulin would be protected from the pro-inflammatory toxic effects of PCB 126.
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:The response of gut microbiota of Brandt's vole to diets supplementation with fructose and fructo-oligose
Project description:At birth, newborns are exposed to gut microbiota, which plays a critical role in host physiology. A reduced level of microbial diversity has been associated with necrotizing enterocolitis (NEC), one of the most deadly diseases in premature infants, but the underlying disease mechanisms are still poorly understood. Although the epithelial turnover of germ free mice is significantly delayed compared to conventionally raised mice, it remains unclear how gut microbiota exposure in the early postnatal period promotes stem cell renewal and differentiation. By analyzing genetic and experimental mouse models and performing single cell analysis, we demonstrate that gut microbiota promotes stem cell differentiation through the activation of critical stromal niche components. Our single cell analysis reveals that gut microbiota controls the size and heterogeneity of macrophage populations that secrete Wnt ligands, thereby maintaining the proliferation of intestinal telocytes, a recently identified gut mesenchymal stem cell niche. We show that stem cell differentiation, when impaired by antibiotic treatment promotes NEC, while treatment with Lactobacillus, which in NEC is dramatically less abundant, rescues NEC-like pathology through the activation of macrophage and telocyte niches. Our work highlights the mechanisms of how gut microbiota-facilitate mesenchymal niche proliferation which supports stem cell differentiation in early postnatal development.
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:Chromosome sequencing of Brandt's vole with different diets
Project description:Intracerebral hemorrhage (ICH) induces alterations in the gut microbiota composition, significantly impacting neuroinflammation post-ICH. However, the impact of gut microbiota absence on neuroinflammation following ICH-induced brain injury remain unexplored. Here, we observed that the gut microbiota absence was associated with reduced neuroinflammation, alleviated neurological dysfunction, and mitigated gut barrier dysfunction post-ICH. In contrast, recolonization of microbiota from ICH-induced SPF mice by transplantation of fecal microbiota (FMT) exacerbated brain injury and gut impairment post-ICH. Additionally, microglia with transcriptional changes mediated the protective effects of gut microbiota absence on brain injury, with Apoe emerging as a hub gene. Subsequently, Apoe deficiency in peri-hematomal microglia was associated with improved brain injury. Finally, we revealed that gut microbiota influence brain injury and gut impairment via gut-derived short-chain fatty acids (SCFA).