Human gut
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ABSTRACT:
PROVIDER: PRJNA779475 | ENA |
REPOSITORIES: ENA
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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:Constipation affects approximately 15% of the global population, and gut microbiota dysbiosis is implicated in its pathogenesis. Rothia mucilaginosa, a commensal bacterium with established anti-inflammatory properties, has not been previously investigated for its effects on intestinal function. In this study, we evaluated the therapeutic potential of R. mucilaginosa in a loperamide-induced constipation mouse model using multiomics approaches. Twenty-six SPF male C57BL/6 mice were divided into normal control (NC, n=8), constipation model control (MC, n=8), and R. mucilaginosa-treated (RG, n=10) groups. R. mucilaginosa intervention significantly improved fecal output and induced gut microbiota remodeling, including enrichment of Akkermansia muciniphila and Alistipes finegoldii. To characterize host molecular responses, RNA-seq was performed on colon tissues to identify differentially expressed genes and pathways associated with constipation alleviation, with particular focus on neuroactive pathway activation.
2026-04-27 | GSE319612 | GEO
Project description:Slow transit constipation (STC) is a complication of depression, which can be commonly seen, that can have a negative impact on STC patients’ prognosis and quality of life. Nonetheless, the pathogenesis of STC is principally uncertain. In this work, colon tissues from STC and non-STC patients were utilized to identify transcriptome expression patterns (mRNAs, lncRNAs, and circRNAs) by high-throughput sequencing.
2026-07-09 | GSE245885 | 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 |