Intestinal microbiota
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA478502 | ENA |
REPOSITORIES: ENA
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Project description:Objectives: Obstructive Sleep Apnea (OSA) is related to repeated upper airway collapse, intermittent hypoxia, and intestinal barrier dysfunction. The resulting damage to the intestinal barrier may affect or be affected by the intestinal microbiota. Methods: A prospective case-control was used, including 48 subjects from Sleep Medicine Center of Nanfang Hospital. Sleep apnea was diagnosed by overnight polysomnography. Fecal samples and blood samples were collected from subjects to detect intestinal microbiome composition (by 16S rDNA gene amplification and sequencing) and intestinal barrier biomarkers – intestinal fatty acid-binding protein (I-FABP) and D-lactic acid (D-LA) (by ELISA and colorimetry, respectively). Results: The severity of OSA was related to differences in the structure and composition of the intestinal microbiome. Enriched Fusobacterium, Megamonasa, Lachnospiraceae_UCG_006, and reduced Anaerostipes was found in patients with severe OSA. Enriched Ruminococcus_2, Lachnoclostridium, Lachnospiraceae_UCG_006, and Alloprevotella was found in patients with high intestinal barrier biomarkers. Lachnoclostridium and Lachnospiraceae_UCG_006 were the common dominant bacteria of OSA and intestinal barrier damage. Fusobacterium and Peptoclostridium was independently associated with apnea-hypopnea index (AHI). The dominant genera of severe OSA were also related to glucose, lipid, neutrophils, monocytes and BMI. Network analysis identified links between the intestinal microbiome, intestinal barrier biomarkers, and AHI. Conclusions: The study confirms that changes in the intestinal microbiota are related to intestinal barrier biomarkers among patients in OSA. These changes may play a pathophysiological role in the systemic inflammation and metabolic comorbidities associated with OSA, leading to multi-organ morbidity of OSA.
2023-08-30 | GSE181270 | GEO
Project description:Despite an established link between sleep deprivation and epigenetic processes in humans, it remains unclear to what extent sleep deprivation modulates DNA methylation. We performed a within subject randomized blinded study with 16 healthy subjects to examine the effect of one night of total acute sleep deprivation (TSD) on the genome wide methylation profile in blood compared to normal sleep. Genome-wide differences in methylation between both conditions were assessed by applying a paired regression model that corrected for monocyte subpopulations (neutrophil/leukocyte ratio). Additionally, the correlations between the methylation of genes detected to be modulated by TSD and gene expression were examined in a separate, publicly available cohort of ten healthy male donors (E-GEOD-49065). Sleep deprivation significantly affected the DNA methylation profile both independently and in dependency of shifts in monocyte composition. Our study detected differential methylation of 269 probes. Notably, one CpG site was located 69bp upstream of ING5, which has been shown to be differentially expressed following sleep deprivation. Gene set enrichment analysis detected the Notch and Wnt signaling pathways to be enriched among the differentially methylated genes. These results provide evidence that total acute sleep deprivation alters the methylation profile in healthy human subjects. This is, to our knowledge, the first study that systematically investigated the impact of total acute sleep deprivation on genome-wide DNA methylation profiles in blood and related the epigenomic findings to the expression data.
2016-06-30 | E-MTAB-4664 | biostudies-arrayexpress
Project description:Purpose: To determine the specific effects of 6 hours sleep deprivation after a learning event on the transcriptomes of microglia. Sleep deprivation can generate inflammatory responses in the neuronal environment. In turn, this inflammation increases sleep drive, leading to a rebound in sleep duration. Microglia, a type of support cell found exclusively in the brain, have previously been found to release of inflammatory signals and exhibit altered characteristics in response to sleep deprivation. Together, this suggests microglia may be partially responsible for the brain’s response to sleep deprivation through their inflammatory activity. In this study, we fully and selectively ablated microglia from the mouse brain and assessed resulting sleep, circadian, and sleep deprivation phenotypes. We find microglia are dispensable for both homeostatic sleep and circadian function and the sleep rebound response to sleep deprivation. However, we uncover a phenomenon by which microglia appear to be essential for the protection of synapses and associated memories formed during a period of sleep deprivation, further expanding the list of known functions for microglia in synaptic modulation.
2021-05-12 | GSE174231 | GEO
Project description:Study Objectives: Sleep deprivation is highly prevalent and caused by conditions such as night shift work or illnesses like obstructive sleep apnea. Compromised sleep is proposed to play a role in several cardiovascular, immune related and neurodegenerative disorders. We recently published human serum proteome changes after a simulated night shift. This study aimed to further explore changes in the human blood serum after 6h of sleep deprivation at night by proteomics and systems biological databases. Methods: Human blood serum samples from 8 self-declared healthy females were analyzed using mass spectrometry and high-pressure liquid chromatography. Each subject was their own control, and two samples were taken from each subject, the first one after 6h of sleep at night and the second one after 6h of sleep deprivation the following night. Biological databases and bioinformatic software were used for systems biological analyzes and comparative analysis with other published sleep-related datasets. Results: Of 494 proteins, 66 were found to be differentially expressed after 6h of sleep deprivation at night. Functional enrichment analysis revealed associations of these proteins with several biological functions related to the regulation of cellular processes like protein- and ion-binding connected to platelet degranulation and blood coagulation, as well as associations with different curated gene sets. Conclusions: This study presents serum proteomic changes after 6h of sleep deprivation, supports previous findings that only 6h of sleep deprivation affects several biological processes and revealed a molecular signature of protein changes related to pathological conditions like altered coagulation and platelet function, impaired lipid and immune function and cancer. Keywords: Human blood serum, proteomics, sleep deprivation, cellular stress, functional enrichment analysis
2024-06-27 | PXD045729 | Pride
Project description:Every day, we sleep for a third of the day. Sleep is important for cognition, brain waste clearance, metabolism, and immune responses. Homeostatic regulation of sleep is maintained by progressively rising sleep need during wakefulness, which then dissipates during sleep. The molecular mechanisms governing sleep are largely unknown. Here, we used a combination of single-cell RNA sequencing and cell-type specific proteomics to interrogate the molecular and functional underpinnings of sleep. Different cell-types in the brain regions show similar transcriptional response to sleep need whereas sleep deprivation changes overall expression indicative of altered antigen processing, synaptic transmission and cellular metabolism in brainstem, cortex and hypothalamus, respectively. Increased sleep need enhances expression of transcription factor Sox2, Mafb, and Zic1 in brainstem; Hlf, Cebpb and Sox9 in cortex, and Atf3, Fosb and Mef2c in hypothalamus. Results from cell-type proteome analysis suggest that sleep deprivation changes abundance of proteins in cortical neurons indicative of altered synaptic vesicle cycles and glucose metabolism whereas in astrocytes it alters the abundance of proteins associated with fatty acid degradation. Similarly, phosphoproteomics of each cell type demonstrates large shifts in site-specific protein phosphorylation in neurons and astrocytes of sleep deprived mice. Our results indicate that sleep deprivation regulates transcriptional, translational and post-translational responses in a cell-specific manner and advances our understanding of the cellular and molecular mechanisms that govern sleep-wake homeostasis in mammals.
2022-10-13 | PXD018334 | Pride
Project description:Sleep insufficiency is associated with various disorders (cardiovascular disease, neurodegenerative diseases, immunological disorders.) but the molecular bases for these associations are largely unknown. We used multiple omics techniques to examine changes in the blood of healthy male and female adults voluntarily subjected to 24 h of sleep deprivation followed by up to one day of recovery with normal sleep routines. Thirty-two (14 males, 18 females) healthy adults 22-27 years old donated fasting blood samples prior to (Day 1) and following (Days 2 and 3) a 24-hour period of sleep deprivation. Blood samples were subjected to cell, biochemical, transcriptomic, proteomic and metabolomic analyses. Multi-omics integration analysis showed that sleep deprivation caused marked molecular changes (46.4% transcript genes, 59.3% proteins and 55.6% metabolites) that had not been restored by Day 2. Transient sleep deprivation had the greatest impact on the immune system and, in particular, on neutrophil-mediated immune processes. Correlation analysis with neutrophils suggested the plasma level of superoxidase dismustase-1 (SOD1) and the primary blood mononuclear cell transcriptional profile of the S100A8 gene could be used as biomarkers reflecting the sleep deprivation-associated disordered immunological state. An increased number of immune cells (leukocytes, neutrophils, monocytes, eosinophils, CD4+T), inflammatory factors (TNF-α, INF-γ, Il-6, IL-10, IL-12) and c-reactive protein in blood plasma further demonstrated the dysregulation of the immune system associated with short-term sleep deprivation. Other important findings associated with sleep deprivation included a significant decrease in the plasma melatonin level and an enrichment of molecules in signaling pathways associated with brain disorders, including schizophrenia and neurodegenerative diseases. Taken in concert, these points suggest that disrupted sleep, such as may occur in shift work, perturbs immunological status and may increase the risk for brain disorders in later life.
2022-04-23 | PXD033402 |
Project description:Disruption of sleep and circadian rhythms are a comorbid feature of many pathologies, and can negatively influence many health conditions, including degenerative disease, metabolic illness, cancer, and various neurological disorders. Genetic association studies linking sleep and circadian disturbances with disease susceptibility have mainly focused on changes in gene expression due to mutations, such as single-nucleotide polymorphisms. The interaction between sleep and/or circadian rhythms with the use of Alternative Polyadenylation (APA) has been largely undescribed, particularly in the context of other disorders. APA is a process that generates various transcript isoforms of the same gene affecting its mRNA translation, stability, localization, and subsequent function. Here we identified unique polyadenylation sites (PASs) expressed in rat brain over time-of-day, immediately following sleep deprivation, and the subsequent recovery period. From these data, we performed a meta-analysis of sleep- or circadian-associated PASs with recently described APA-linked brain disorder susceptibility genes.
2023-12-25 | GSE250324 | GEO
Project description:Using Drosophila we identified a glia-secreted antimicrobial peptide IM33, which alters gut microbiota to modulate sleep. To understand how the gut commensal Lactiplantibacillus plantarum functions in the brain to regulate sleep, we performed single-cell RNA sequencing.
2023-07-21 | GSE185369 | GEO
Project description:<p>Chronic sleep loss profoundly impacts metabolic health and shortens lifespan, but studies of the mechanisms involved have focused largely on acute sleep deprivation. To identify metabolic consequences of chronically reduced sleep, we conducted unbiased metabolomics on heads of three adult Drosophila short-sleeping mutants with very different mechanisms of sleep loss: fumin (fmn), redeye (rye), and sleepless (sss). Common features included elevated ornithine and polyamines, with lipid, acyl-carnitine, and TCA cycle changes suggesting mitochondrial dysfunction. Studies of excretion demonstrate inefficient nitrogen elimination in adult sleep mutants, likely contributing to their polyamine accumulation. Increasing levels of polyamines, particularly putrescine, promote sleep in control flies but poison sleep mutants. This parallels the broadly enhanced toxicity of high dietary nitrogen load from protein in chronically sleep-restricted Drosophila, including both sleep mutants and flies with hyper-activated wake-promoting neurons. Together, our results implicate nitrogen stress as a novel mechanism linking chronic sleep loss to adverse health outcomes-and perhaps for linking food and sleep homeostasis at the cellular level in healthy organisms.</p>
2023-03-18 | MTBLS3318 | MetaboLights