Ontology highlight
ABSTRACT:
PROVIDER: PRJNA429372 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6458060_1.fastq.gz | Fastqsanger.gz | |||
| SRR6458060_2.fastq.gz | Fastqsanger.gz | |||
| SRR6458061_1.fastq.gz | Fastqsanger.gz | |||
| SRR6458061_2.fastq.gz | Fastqsanger.gz | |||
| SRR6458052_1.fastq.gz | Fastqsanger.gz |
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Project description:To investigate effects of long-term intake of RPS on gene expression in the colon and liver of pigs,thirty-six Duroc × Landrace × Large White growing barrows were randomly allocated to corn starch (CS) and RPS groups. Each group consisted of six replicates (pens), with three pigs per pen. Pigs in the CS group were offered a corn/soybean-based diet, while pigs in the RPS group were put on a diet in which 230 g/kg (growing period) or 280 g/kg (finishing period) purified corn starch was replaced with purified RPS during a 100-day trial. Liver transcriptomic results showed that the expression of CD36, CPT1B and ACADM was down-regulated, while AGPAT4, GPAT, FABP1 and FABP3 were up-regulated by the RPS diet, indicating a decrease in fatty acid intake and synthesis, and an increase in fatty acid oxidation and glycerophospholipid synthesis.Analysis of the colonic transcriptome profiles revealed that the RPS diet changed the colonic expression profile of the host genes mainly involved in immune response pathways. RPS significantly increased proinflammartory cytokine IL-1? gene expression and suppressed genes involved in lysosome. Thirty-six Duroc × Landrace × Large White growing barrows (70 days of age, 23.78 ± 1.87 kg) were randomly allocated to two groups, each group consisting of three pigs per pen, and six replicates. Pigs in the control group were offered a corn/soybean-based diet, while 230 g/kg purified corn starch (CS) was replaced with purified RPS in the RPS diet group. Diets were formulated according to the nutrient requirements of the National Research Council (1998). When animals reached the age of 120 days, diets were adapted to the nutrient requirements of the animals (finishing diet) and the amount of purified starch increased to 280 g of CS or RPS per kilogram of feed. Pigs had unlimited access to feed and water throughout the experimental period, which consisted of two 50-day trials in which the pigs consumed the growing diet (days 0-50) and finishing diet (days 51-100), respectively. On day 100, one pig from each replicate that met the target slaughter weight (105 to 110 kg) was slaughtered. The liver and colonic mucosa tissues were collected and preserved in liquid nitrogen for gene expression analysis.
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Project description:The aim of this study was to investigate whether long term intake of pea fiber would improve colonic barrier, bacterial profile and alter colonic gene expression using DNA microarray. Fifty weaned pigs were randomly allocated into 2 groups receiving control and fibrous diet with inclusion of pea fiber from weaning age until d 160. The two diets had similar nutrient levels. Pigs fed pea fiber diet (PF diet) had markedly decreased overall average daily feed intake (ADFI) and Feed:Gain in growing and finishing period (P<0.05). In addition, long term intake of PF diet induced deeper crypt (+50 %, P<0.05), increased protein expression of colonic mucin and sIgA (+13～16 %, P<0.05). Resulting from the increased lactobacillus content (P<0.05), moreover, pigs fed PF diet had significantly higher concentration of colonic total short chain fatty acid (SCFA) and acetic acid. DNA microarray results indicated that feeding PF diet induced alterations in the expression of colonic cancer, immune response and lipid metabolism-related genes, as well as genes involved in signal pathway such as intestinal immune network for IgA production, PPAR signaling pathway and nutrient metabolism-related pathways. Collectively, our results suggested that long term intake of PF diet would improve colonic health via altering colonic bacteria profile, colonic barriers, immune and metabolism related protein or gene expressions. A total of 50 weaned pigs (Duroc×Landrace×Yorkshire, initial body weight: 7.2±0.5 kg) were randomly allocated to 2 groups with 5 pens each group and 5 pig each pen. Pigs were fed control (Control) and fibrous diets (10～20 % inclusion of pea fiber, PF) from weaning at 28 day to 160 day-old-age, which is subjected to phase feeding by weaning diet (weaning to d 30 post-weaning), growing diet (d 30～90 postweaning) and finishing diet (d 90～160 postweaning) according to their physiological stage. At d 160 postweaning, four pigs each group were selected to be slaughtered for collection of colonic tissues and DNA microarray was applied to the colonic tissues for analysis of gene expression.
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Project description:"Shigella spp. are the causative agents of shigellosis, which remains a major cause of death in children under the age of five. Shigellosis is marked by fever and leads to hemorrhagic diarrhea; Shigella bacteremia are reported in more severe cases. These clinical features strongly suggest that Shigella survive to plasma exposure, although it has not been previously investigated at a molecular level. In this report, we confirmed in a guinea pig model of shigellosis that local hemorrhages were induced by S. flexneri 5a and S. sonnei and we demonstrated that Shigella reached CD31+/CD34+ blood vessels within the mucosa during late infection stage and further disseminated in the blood circulation. These results confirmed the exposition of Shigella to plasma components during its virulence cycle, from the hemorrhagic colonic mucosa to the blood circulation. We demonstrated that all tested Shigella strains survived to plasma exposure in vitro and we have shown that Serine Protease Autrotransporters of Enterobacteriaceae (SPATEs) are essential for Shigella dissemination within the colonic mucosa and in the blood circulation. We confirmed that SPATEs were expressed and secreted within poorly oxygenated environments encountered by Shigella from hypoxic foci of infection to the blood circulation. We have further demonstrated that SPATEs promoted the survival of Shigella to plasma exposure, by cleaving the complement 3 component (C3), hence impairing the complement system activation."
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