Project description:<p>In order to create a melanocyte-specific eQTL resource, we obtained primary human melanocyte cultures isolated from foreskin of 106 healthy newborn males predominantly of European descent. Melanocytes were cultured in lot-matched culture medium in randomized batches to minimize variability that could be introduced by culturing conditions. RNA sequencing and direct SNP genotyping of these samples produced an average of ~87.9 million reads (paired-end, stranded, 126bps), and ~713,000 SNP genotypes, respectively.</p>
Project description:Three human gut microbiome samples from different individuals were cultured in an optimized culture medium with or without the presence of different sugars (10 mM glucose, 20 mM fructose, 10 mM glucose + 20 mM fructose, or 10 mM kestose). Samples were cultured in technical triplicates, and were taken at 0 hr, 1hr, 5 hr, 12 hr and 24 hr of culturing for optical density and metaproteomic analyses. Cultured microbiota cells were subjected to metaproteomics analysis using LC-MS/MS and a TMT approach.
Project description:We aimed to investigate the microbial community composition in patients with intracerebral hemorrhage (ICH) and its effect on prognosis. The relationship between changes in bacterial flora and the prognosis of spontaneous cerebral hemorrhage was studied in two cohort studies. Fecal samples from healthy volunteers and patients with intracerebral hemorrhage were subjected to 16S rRNA sequencing at three time points: T1 (within 24 hours of admission), T2 (3 days post-surgery), and T3 (7 days post-surgery) using Illumina high-throughput sequencing technology.
Project description:To explore the regulatory mechanism of intestinal flora in Citrobacter rodentium -induced intestinal infection by transcriptome analysis at miRNA molecular level.
Project description:Germ-free (GF) mice can be used as a powerful tool to investigate the role of the intestinal commensal flora in metabolism and immune tolerance. In this study we have used whole genome transcriptome analyses to compare expression levels systemically in liver of germ-free mice and specific pathogen free (SPF) mice. Keywords: Mouse liver tissue germ-free or specific pathogen free vs universal mouse reference Specific Pathogens Excluded from the SPF mice: Virus 1. Mouse Hepatitis Virus (MHV) 2. Mouse Rotavirus (EDIM) 3. Parvoviruses Minute virus of mice (MVM) Mouse parvo virus (MPV) 4. Pneumonia virus of mice (PVM) 5. Sendai virus 6. Theiler's encephalomyelitis virus 7. Ectromelia virus 8. Lymphocytic choriomeningitis virus (LCMV) 9. Mouse adenovirus 10. Mouse cytomegalovirus 11. Reovirus type 3 Bacteria 1. Citrobacter rodentium 2. Clostridium piliforme (Tyzzer’s disease) 3. Corynebacterium kutscheri 4. Mycoplasma pulmonis 5. Pasteurellaceae 6. Salmonella spp. 7. Streptococci-β-haemolytic 8. Streptococcus pneumoniae 9. Helicobacter spp. 10. Streptobacillus moniliformis Parasite 1. Ectoparasites 2. Endoparasites
Project description:Environmental Enteric Dysfunction (EED) is a chronic inflammatory condition of the intestine characterized by villus blunting, compromised intestinal barrier function, and reduced nutrient absorption. Here, we show that key genotypic and phenotypic features of EED-associated intestinal injury can be reconstituted in a human intestine-on-a-chip (Intestine Chip) microfluidic culture device lined by organoid-derived intestinal epithelial cells from EED patients and cultured in nutrient deficient medium lacking niacinamide and tryptophan (-N/-T). Exposure of EED Intestine Chips to -N/-T deficiencies resulted in transcriptional changes similar to those seen in clinical EED patient samples including congruent changes in six of the top ten upregulated genes. Exposure of EED Intestine Chips or chips lined by healthy intestinal epithelium (healthy Intestine Chips) to -N/-T medium resulted in severe villus blunting and barrier dysfunction, as well as impairment of fatty acid uptake and amino acid transport.
Project description:Irritable Bowel Syndrome (IBS) is a disorder of the gut-brain axis, characterized by altered gut function and frequent psychiatric co-morbidity. Although altered intestinal microbiome profiles have been documented, their relevance to the clinical expression of IBS is unknown. To evaluate a functional role of the microbiota, we colonized germ-free mice with fecal microbiota from healthy controls or IBS patients with accompanying anxiety, and monitored gut function and behavior. Mouse microbiota profiles clustered according to their human donors. Despite having taxonomically similar composition as controls, mice with IBS microbiota had distinct serum metabolomic profiles related to neuro- and immunomodulation. Mice with IBS, but not control microbiota, exhibited faster gastrointestinal transit, intestinal barrier dysfunction, innate immune activation and anxiety-like behavior. These results support the notion that the microbiota contributes to both intestinal and behavioral manifestations of IBS and rationalize the use of microbiota-directed therapies in ameliorating IBS.
Project description:Aims: Atorvastatin is a commonly used cholesterol-lowering drug that possesses non-canonical anti-inflammatory properties. However, the precise mechanism underlying its anti-inflammatory effects remains unclear. Materials and methods: The acute phase of ulcerative colitis (UC) was induced using a 5 % dextran sulfate sodium (DSS) solution for 7 consecutive days and administrated with atorvastatin (10 mg/kg) from day 3 to day 7. mRNA-seq, histological pathology, and inflammatory response were determined. Intestinal microbiota alteration, tryptophan, and its metabolites were analyzed through 16S rRNA sequencing and untargeted metabolomics. Key findings: Atorvastatin relieved the DSS-induced UC in mice, as evidenced by colon length, body weight, disease activity index score and pathological staining. Atorvastatin treatment reduced the level of pro_x0002_inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α). Atorvastatin also relieved the intestinal microbiota disorder caused by UC and decreased the proliferation of pernicious microbiota such as Akkermansia and Bacteroides. Atorvastatin dramatically altered tryptophan metabolism and increased the fecal contents of tryptophan, indolelactic acid (ILA), and indole-3-acetic acid (IAA). Furthermore, atorvastatin enhanced the expression level of aryl hydrocarbon receptor (AhR) and interleukin-22 (IL-22) and further promoted the expression level of intestinal tight junction proteins, such as ZO-1 and occludin, in colitis mice. Significance: These findings indicated that atorvastatin could alleviate UC by regulating intestinal flora disorders, promoting microbial tryptophan metabolism, and repairing the intestinal barrier.