Ontology highlight
ABSTRACT:
PROVIDER: PRJNA781055 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16961800_1.fastq.gz | Fastqsanger.gz | |||
| SRR16961800_2.fastq.gz | Fastqsanger.gz | |||
| SRR16961801_1.fastq.gz | Fastqsanger.gz | |||
| SRR16961801_2.fastq.gz | Fastqsanger.gz | |||
| SRR16961802_1.fastq.gz | Fastqsanger.gz |
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Project description:Chronic diseases arise when pathophysiological processes achieve a steady state by self-reinforcing. Here, we explored the possibility of a self-reinforcement state in a common condition, chronic constipation, where alterations of the gut microbiota have been reported. The functional impact of the microbiota shifts on host physiology remains unclear, however we hypothesized that microbial communities adapted to slow gastrointestinal transit affect host functions in a way that reinforces altered transit, thereby maintaining the advantage for microbial self-selection. To test this, we examined the impact of pharmacologically (loperamide)-induced constipation (PIC) on the structural and functional profile of altered gut microbiota. PIC promoted changes in the gut microbiome, characterized by decreased representation of butyrate-producing Clostridiales, decreased cecal butyrate concentration and altered metabolic profiles of gut microbiota. PIC-associated gut microbiota also impacted colonic gene expression, suggesting this might be a basis for decreased gastrointestinal (GI) motor function. Introduction of PIC-associated cecal microbiota into germ-free (GF) mice significantly decreased GI transit time. Our findings therefore support the concept that chronic diseases like constipation are caused by disease-associated steady states, in this case, caused by reciprocating reinforcement of pathophysiological factors in host-microbe interactions. We used microarrays to detail the global gene expression profile in the proximal colon smooth muscle tissues of germ-free, conventionalized, or specific pathogen free mouse C57Bl/6 female and male specific pathogen free (SPF) mice were bred and housed in the animal care facility at the University of Chicago. Mice of 8–10 weeks of age were treated with 0.1% loperamide in the drinking water for 7 days. Age matched, germ-free (GF) C57Bl/6 mice were gavaged orally with cecal luminal contents harvested from control or loperamide-treated C57Bl/6 donor mice. Recipient mice were sacrificed 4 weeks post-colonization.
2014-07-12 | E-GEOD-59320 | biostudies-arrayexpress
Project description:Chronic diseases arise when pathophysiological processes achieve a steady state by self-reinforcing. Here, we explored the possibility of a self-reinforcement state in a common condition, chronic constipation, where alterations of the gut microbiota have been reported. The functional impact of the microbiota shifts on host physiology remains unclear, however we hypothesized that microbial communities adapted to slow gastrointestinal transit affect host functions in a way that reinforces altered transit, thereby maintaining the advantage for microbial self-selection. To test this, we examined the impact of pharmacologically (loperamide)-induced constipation (PIC) on the structural and functional profile of altered gut microbiota. PIC promoted changes in the gut microbiome, characterized by decreased representation of butyrate-producing Clostridiales, decreased cecal butyrate concentration and altered metabolic profiles of gut microbiota. PIC-associated gut microbiota also impacted colonic gene expression, suggesting this might be a basis for decreased gastrointestinal (GI) motor function. Introduction of PIC-associated cecal microbiota into germ-free (GF) mice significantly decreased GI transit time. Our findings therefore support the concept that chronic diseases like constipation are caused by disease-associated steady states, in this case, caused by reciprocating reinforcement of pathophysiological factors in host-microbe interactions. We used microarrays to detail the global gene expression profile in the proximal colon smooth muscle tissues of germ-free, conventionalized, or specific pathogen free mouse
2014-07-12 | GSE59320 | GEO
Project description:Protective effect of Golden Bifid treatment on slow transit constipation rat
| PRJNA1141165 | ENA
Project description:Efficacy of a Postbiotic and its Components in Promoting Colonic Transit and Alleviating Chronic Constipation in Humans and Mice
2025-03-28 | PXD062407 |
Project description:<p>A rat model of slow transit constipation (STC) was induced by loperamide hydro-chloride to explore the therapeutic mechanism of Zingiber mioga (Thunb.) Rosc. (RH) using integrated metabolomic and metagenomic approaches. Thirty-six Sprague–Dawley (SD) rats were randomly assigned to 6 groups (n = 6): the con-trol group, model group, mosapride-positive control group (2 mg kg−1), and RH low- (1,350 mg kg−1), medium- (2,700 mg kg−1), and high-dose (3,400 mg kg−1) groups. The STC model was established by intragastric administration of lop-eramide hydrochloride (5 mg/kg) for 35 consecutive days, with simultaneous drug intervention. Serum levels of substance P (SP), motilin (MTL), and gastrin (GAS) were quantified; colonic pathological sections were prepared; and serum untargeted metabolomics and fecal metagenomics analyses were conducted. Key findings demonstrated that RH significantly decreased serum SP levels while elevating MTL and GAS levels in STC rats, attenuated colonic pathological lesions, and increased intestinal propulsion rate. Serum metabolomics analysis identified 15 differential metabolites, which were primarily involved in nitrogen metabolism, neuroactive ligand-receptor interaction, and amino acid metabo-lism. Fecal metagenomics analysis revealed that RH restored the Eubacteriales/ Lachnospirales ratio and increased the relative abundance of probiotic genera (e.g., Ruminococcus sp., Eubacterium sp.). In conclusion, RH exerts laxative effects in STC rats by regulating gastrointestinal hormones, mitigating colonic injury, and accelerating intestinal peristalsis. These effects may be mediated by ameliorating amino acid and nitrogen metabolic disorders and modulating gut microbiota composition. </p>
2026-02-11 | MTBLS13888 | MetaboLights