Project description:Oral administration of an extract of compost fermented with thermophiles to pigs reduces the incidence of stillbirth and promotes piglet growth. However, the mechanism by which compost extract modulates the physiological conditions of the animals remains largely unknown. Here, we investigate the effects of compost extract on the gene expression in the intestine of the rat as a mammalian model. Gene expression analyses of the intestine indicated that several immune-related genes were upregulated following compost exposure. Thus, thermophile-fermented compost can contain microbes and/or substances that activate the gut mucosal immune response in the rat. In Male Wistar rats aged 3 weeks, tap water was supplemented with 1.0% (v/v) compost extract for the experimental rats, whereas water only was given to the control rats. The rats received water ad libitum for 12 weeks. Fresh gut samples were collected from individual rats at the end of the feeding test and stored at -80°C. The intestine were separated from the gut and used as samples for the isolation of total RNA. otal RNA was then subjected to microarray experiments using the Whole Rat Genome (4x44k) Oligo Microarray (Agilent Technologies, Inc.)
Project description:HuMiChip was used to analyze human oral and gut microbiomes, showing significantly different functional gene profiles between oral and gut microbiome.
2014-02-04 | GSE54290 | GEO
Project description:Gut microbiome of rats after oral SrR
Project description:HuMiChip was used to analyze human oral and gut microbiomes, showing significantly different functional gene profiles between oral and gut microbiome. The results were used to demonstarte the usefulness of applying HuMiChip to human microbiome studies.
Project description:In order to gain insight into gene regulation in the Drosophila gut following oral infection, we performed the genome-wide DNA Polymerase II binding data for Polymerase II in the fly gut.
Project description:Background Alterations of the gut microbiome have been linked to multiple chronic diseases. However, the drivers of such changes remain largely unknown. The oral cavity acts as a major route of exposure to exogenous factors including pathogens, and processes therein may affect the communities in the subsequent compartments of the gastrointestinal tract. Here, we perform strain-resolved, integrated multi-omic analyses of saliva and stool samples collected from eight families with multiple cases of type 1 diabetes mellitus (T1DM). Results We identified distinct oral microbiota mostly reflecting competition between streptococcal species. More specifically, we found a decreased abundance of the commensal Streptococcus salivarius in the oral cavity of T1DM individuals, which is linked to its apparent competition with the pathobiont Streptococcus mutans. The decrease in S. salivarius in the oral cavity was also associated with its decrease in the gut as well as higher abundances in facultative anaerobes including Enterobacteria. In addition, we found evidence of gut inflammation in T1DM as reflected in the expression profiles of the Enterobacteria as well as in the human gut proteome. Finally, we were able to follow transmitted strain-variants from the oral cavity to the gut at the metagenomic, metatranscriptomic and metaproteomic levels, highlighting not only the transfer, but also the activity of the transmitted taxa along the gastrointestinal tract. Conclusions Alterations of the oral microbiome in the context of T1DM impact the microbial communities in the lower gut, in particular through the reduction of “oral-to-gut” transfer of Streptococcus salivarius. Our results indicate that the observed oral-cavity-driven gut microbiome changes may contribute towards the inflammatory processes involved in T1DM. Through the integration of multi-omic analyses, we resolve strain-variant “mouth-to-gut” transfer in a disease context.
Project description:Interleukin (IL)-23 and IL-17 are well-validated therapeutic targets in autoinflammatory diseases. Antibodies targeting IL-23 and IL-17 have shown clinical efficacy but are limited by high costs, safety risks, lack of sustained efficacy, and poor patient convenience as they require parenteral administration. Here, we present designed miniproteins inhibiting IL-23R and IL-17 with antibody-like, low picomolar affinities at a fraction of the molecular size. The minibinders potently block cell signaling in vitro and are extremely stable, enabling oral administration and low-cost manufacturing. The orally administered IL-23R minibinder shows efficacy better than a clinical anti-IL-23 antibody in mouse colitis and has a favorable pharmacokinetics (PK) and biodistribution profile in rats. This work demonstrates that orally administered de novo-designed minibinders can reach a therapeutic target past the gut epithelial barrier. With high potency, gut stability, and straightforward manufacturability, de novo-designed minibinders are a promising modality for oral biologics.