Project description:Modulation of dysbiotic mice gut microbial diversity after supplementation of pectic oligosaccharide (POS) based synbiotic formulation Raw sequence reads
Project description:Morphine and its pharmacological derivatives are the most prescribed analgesics for moderate to severe pain management. However, chronic use of morphine reduces pathogen clearance and induces bacterial translocation across the gut barrier. The enteric microbiome has been shown to play a critical role in the preservation of the mucosal barrier function and metabolic homeostasis. Here, we show for the first time, using bacterial 16s rDNA sequencing, that chronic morphine treatment significantly alters the gut microbial composition and induces preferential expansion of the gram-positive pathogenic and reduction of bile-deconjugating bacterial strains. A significant reduction in both primary and secondary bile acid levels was seen in the gut, but not in the liver with morphine treatment. Morphine induced microbial dysbiosis and gut barrier disruption was rescued by transplanting placebo-treated microbiota into morphine-treated animals, indicating that microbiome modulation could be exploited as a therapeutic strategy for patients using morphine for pain management. In this study, we establish a link between the two phenomena, namely gut barrier compromise and dysregulated bile acid metabolism. We show for the first time that morphine fosters significant gut microbial dysbiosis and disrupts cholesterol/bile acid metabolism. Changes in the gut microbial composition is strongly correlated to disruption in host inflammatory homeostasis13,14 and in many diseases (e.g. cancer/HIV infection), persistent inflammation is known to aid and promote the progression of the primary morbidity. We show here that chronic morphine, gut microbial dysbiosis, disruption of cholesterol/bile acid metabolism and gut inflammation; have a linear correlation. This opens up the prospect of devising minimally invasive adjunct treatment strategies involving microbiome and bile acid modulation and thus bringing down morphine-mediated inflammation in the host.
Project description:A. thaliana lines with reduced lignin content through down-regulation of the lignin biosynthesis enzymes cinnamoyl CoA reductase (CCR) exhibit extensive cell wall remodeling which results in the release of a mixture of pectic oligosaccharide elicitors of pathogenesis-related (PR) protein gene expression through the salicylic acid signaling pathway. Loss of function of FERONIA, a CrRLK1-like subfamily receptor-like kinase resulted in loss of PR-1, -2 and- 5 gene activation in stems of the ccr1/fer-4 double mutant.
Project description:In the presented study, in order to unravel gut microbial community multiplicity and the influence of maternal milk nutrients (i.e., IgA) on gut mucosal microbiota onset and shaping, a mouse GM (MGM) was used as newborn study model to discuss genetic background and feeding modulation on gut microbiota in term of symbiosis, dysbiosis and rebiosis maintenance during early gut microbiota onset and programming after birth. Particularly, a bottom-up shotgun metaproteomic approach, combined with a computational pipeline, has been compred with a culturomics analysis of mouse gut microbiota, obtained by MALDI-TOF mass spectrometry (MS).
Project description:Opioid analgesics are frequently prescribed in the United States and worldwide. However, serious side effects such as addiction, immunosuppression and gastrointestinal symptoms limit long term use. In the current study using a chronic morphine-murine model a longitudinal approach was undertaken to investigate the role of morphine modulation of gut microbiome as a mechanism contributing to the negative consequences associated with opioids use. The results revealed a significant shift in the gut microbiome and metabolome within 24 hours following morphine treatment when compared to placebo. Morphine induced gut microbial dysbiosis exhibited distinct characteristic signatures profiles including significant increase in communities associated with pathogenic function, decrease in communities associated with stress tolerance. Collectively, these results reveal opioids-induced distinct alteration of gut microbiome, may contribute to opioids-induced pathogenesis. Therapeutics directed at these targets may prolong the efficacy long term opioid use with fewer side effects.
Project description:The aim of this study was to investigate the causative effect of CS induced dysbiosis on obesity and insulin resistance in a high-fat diet induced obese (DIO) mouse model. Male germ-free BALB/c mice were humanized by fecal microbiota transfer using samples from children born by CS or VD and fed HFD for 16 weeks. Adipose tissue was sampled for RNAseq at study termination.
Project description:We profiled microRNA expression in brain and colon tissues from a mouse model of ischemic stroke comorbid with gut dysbiosis after Xinqingning Tablet treatment.