Project description:We collected caecal contents from 30 chickens divided into 5 groups (6 birds per group) with each group receiving different quantity of soluble inulin and insoluble cellulose. We isolated DNA, RNA, and proteins to perform metagenomics, metatranscriptomics, and metaproteomics analysis, respectively.
Project description:Objective: To explore the role of GPR15L in the pathogenesis of experimental colitis and IBD. Design: We studied how genetic deletion or overexpression of Gpr15l as well as rectal application of recombinant GPR15L alter the course of acute dextran sodium sulfate (DSS) colitis. Rag1-/- and Gpr15-/- mice were used to investigate the role of T cells and Gpr15 for Gpr15l-dependent effects in acute DSS and T cell transfer colitis, respectively. The impact of GPR15L on microbiota was explored with co-housing, littermate and fecal microbiota transfer studies, by 16S rRNA sequencing as well as anti-microbial assays and anaerobic cultures of human stool suspensions analyzed by shotgun metagenomics. The expression of GPR15L was evaluated across three independent cohorts of patients with IBD and correlated to microbial diversity and flare-free survival. Results: Gpr15l clearly mitigated experimental colitis, but this was independent of T cell recruitment and Gpr15. Instead, we observed that the effects of Gpr15l were mediated by altered microbiomes in the large intestine and, consistently, showed that Gpr15l acts as an antimicrobial peptide under anaerobic conditions and shapes microbial communities towards a homeostatic phenotype. Rectal supplementation of Gpr15l counteracted experimental colitis. In patients with IBD, GPR15L expression was decreased in active inflammation, correlated with microbial diversity and was associated with flare-free survival. Conclusions: GPR15L is a host-defense peptide that plays a beneficial role in the pathogenesis of intestinal inflammation. It seems promising to further evaluate its potential as a future therapeutic approach in IBD.
Project description:Campylobacter jejuni is the major cause of acute gastroenteritis in the developed world. It is usually acquired through contaminated poultry as C. jejuni causes a silent asymptomatic infection of the chicken. Pathogens face different sources of stress during its transit through the gut. In this study, we describe the ability of C. jejuni to survive nitrosative stress at very low oxygen levels that reflect those in hypoxic gut environments. Specifically, we here explore an innovative model of signal recognition during colonization. We use a diffusion capsule to feed small, diffusible molecules from chicken caecal matter into a microaerobic C. jejuni culture to study the transcriptomic changes mounted as response to chemical signals present in the chicken gut. We find that in early stages of exposure to the caecal contents (10 min) the dual component colonization regulator, dccR, plays an important yet not fully understood role. Although the caecal material contains cyanide derived from plant sources, we find no role for a truncated globin (encoded by ctb), which has previously been implicated in resistance to this haem ligand.
Project description:EMG produced TPA metagenomics assembly of the Metagenomic, Metatranscriptomic and Metviriomic analysis of samples collected at four time points during a single day at the Gulf of Aqaba in the Red Sea. (Red Sea Diel) data set
Project description:We compared the microbiota of paired mouse caecal contents and faeces by applying a multi-omic approach, including 16S rDNA sequencing, shotgun metagenomics, and shotgun metaproteomics. The aim of the study was to verify whether faecal samples are a reliable proxy for the mouse colonic luminal microbiota, as well as to identify changes in taxonomy and functional activity between caecal and faecal microbial communities, which have to be carefully considered when using stool as sample for mouse gut microbiota investigations.