Project description:We used single-cell RNA sequencing to characterize the heterogeneity duodenal tissue in healthy and chronic inflammatory enteropathy (CIE) affected dogs.
Project description:In small animals, diarrhoea is a regular presentation, the aetiology of which can be varied, from an isolated self-limiting event to more serious episodes requiring symptomatic and supportive treatment. Chronic diarrhoea, defined as diarrhoea lasting longer than 3 weeks, is a relatively common problem often prompting referral for more detailed investigation. Although the potential cause of chronic diarrhoea includes chronic intestinal parasitism and alimentary neoplasia (specifically lymphoma), the majority of these dogs will be diagnosed with idiopathic canine chronic enteropathy (CCE), previously referred to as idiopathic inflammatory bowel disease (IBD). Of those cases diagnosed with CCE, further subdivision based on response to treatment trials leads to a final diagnosis of antibiotic responsive diarrhoea (ARD), food responsive diarrhoea (FRD) or idiopathic inflammatory bowl disease (IBD). The aim of this study was to compare the proteomes of faeces of dogs with chronic enteropathies and a population of healthy dogs, and furthermore to identifying proteins that might be useful in distinguishing FRD from ARD from IBD.
2022-08-29 | PXD017454 | Pride
Project description:Immunoglobulin coating in healthy dogs and dogs with chronic enteropathy
Project description:We developed a non-invasive ex vivo HT29 cell-based minimal model to fingerprint the mucosa-associated microbiota fraction in humans. HT29 cell-associated fractions were characterized by the universal phylogenetic array platform HTF-Microbi.Array, both in presence or in absence of a TNF-M-NM-1-mediated pro-inflammatory stimulus. A high taxonomical level fingerprint profiling of the mucosa-associated microbiota was performed on a group of 12 breast-fed infants and 6 adults (used as controls). Relative abundance of the bacterial species was assessed by using a so-called HTF-Microbi.Array, based on a ligation detection reaction (LDR) - Univerasal array (UA) assay, capable of correctly identify up to 31 intestinal bacterial groups, covering up to 95% of the human gut microbiota
Project description:Build a collection of fecal microbiota in order to determine the characteristics of gut microbiota associated with colorectal cancer in Inflammatory bowel disease (IBD).
Project description:Aconitate decarboxylase 1 (ACOD1) is the enzyme synthesizing itaconate, an immuno-regulatory metabolite tuning host-pathogen interactions. Such functions are achieved by affecting metabolic pathways regulating inflammation and microbe survival. However, at the whole-body level, metabolic roles of itaconate remain largely unresolved. By using multiomics-integrated approaches, here we show that ACOD1 responds to high-fat diet consumption in mice by promoting gut microbiota alterations supporting metabolic disease. Genetic disruption of itaconate biosynthesis protects mice against obesity, alterations in glucose homeostasis and liver metabolic dysfunctions by decreasing meta-inflammatory responses to dietary lipid overload. Mechanistically, fecal metagenomics and microbiota transplantation experiments demonstrate such effects are dependent on an amelioration of the intestinal ecosystem composition, skewed by high-fat diet feeding towards obesogenic phenotype. In particular, unbiased fecal microbiota profiling and axenic culture experiments point towards a primary role for itaconate in inhibiting growth of Bacteroidaceae and Bacteroides, family and genus of Bacteroidetes phylum, the major gut microbial taxon associated with metabolic health. Specularly to the effects imposed by Acod1 deficiency on fecal microbiota, oral itaconate consumption enhances diet-induced gut dysbiosis and associated obesogenic responses in mice. Unveiling an unrecognized role of itaconate, either endogenously produced or exogenously administered, in supporting microbiota alterations underlying diet-induced obesity in mice, our study points ACOD1 as a target against inflammatory consequences of overnutrition.
Project description:The human intestinal microbiota plays an essential role in host health. Modifications in its composition and diversity could induce pathologies such as inflammatory bowel diseases (IBD). These diseases are characterized by an unbalanced intestinal microbiota (a process known as dysbiosis) and an altered immune response. Faecalibacterium prausnitzii, the most abundant commensal bacterium in the human intestinal microbiota of healthy individuals (representing more than 5% of the total bacterial population), has been reported to be lower in feces and mucosa-associated microbiota of IBD patients. In addition, we have shown that both F. prausnitzii and its culture supernatant (SN) have anti-inflammatory and protective effects in both acute and chronic colitis models. However, the host molecular mechanisms involved in these anti-inflammatory effects remain unknown. In order to address this issue, we performed DNA chip-based transcriptomic analyses in HT-29 human intestinal epithelial cells stimulated with TNF-a and exposed to F. prausnitzii SN or to BHI (growth medium for F prausnitzii).