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ABSTRACT:
PROVIDER: PRJNA1102920 | 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:To investigate the pathogenesis of slow transit constipation (STC), we have employed microarray-based miRNA analysis as a discovery platform to identify miRNAs potentially related with STC pathogenesis.Full-thickness specimens were obtained from colons of STC patients undergoing total colectomy and ileorectal anastomosis or subtotal colectomy with antiperistaltic cecoproctostomy. And patients undergoing radical surgery for non-obstructing colon cancer (left colon cancer) as control. These patients were not constipated and had no colonic dilatation. The control specimens were obtained at least 5 cm from the resection margin in tumor free areas. Expression of five miRNAs (miRNA-128, miRNA-129-3p, miRNA-20b,miRNA-27b and miRNA-30b) from this signature was identified by arbitrarily setting the threshold at a fold change of 1.3 or above combined with p < 0.05 in the same RNA samples. Expression of miRNAs in the colon may be involved in STC pathogenesis. The samples were obtained and washed with cold PBS, transported in liquid nitrogen and immediately stored in liquid nitrogen after removal. Total RNA was isolated from frozen histologic specimens using a mirVana™ RNA isolation Kit.
2014-05-27 | E-GEOD-57969 | biostudies-arrayexpress
Project description:To investigate the pathogenesis of slow transit constipation (STC), we have employed microarray-based miRNA analysis as a discovery platform to identify miRNAs potentially related with STC pathogenesis.Full-thickness specimens were obtained from colons of STC patients undergoing total colectomy and ileorectal anastomosis or subtotal colectomy with antiperistaltic cecoproctostomy. And patients undergoing radical surgery for non-obstructing colon cancer (left colon cancer) as control. These patients were not constipated and had no colonic dilatation. The control specimens were obtained at least 5 cm from the resection margin in tumor free areas. Expression of five miRNAs (miRNA-128, miRNA-129-3p, miRNA-20b,miRNA-27b and miRNA-30b) from this signature was identified by arbitrarily setting the threshold at a fold change of 1.3 or above combined with p < 0.05 in the same RNA samples. Expression of miRNAs in the colon may be involved in STC pathogenesis.
2014-05-27 | GSE57969 | GEO