Ontology highlight
ABSTRACT:
PROVIDER: PRJNA817426 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18399516.fastq.gz | Fastqsanger.gz | |||
| SRR18399517.fastq.gz | Fastqsanger.gz | |||
| SRR18399518.fastq.gz | Fastqsanger.gz | |||
| SRR18399519.fastq.gz | Fastqsanger.gz | |||
| SRR18399520.fastq.gz | Fastqsanger.gz |
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Project description:Dendritic cell immunoreceptor (DCIR; Clec4a2), a member of the C-type lectin receptor family, plays important roles in homeostasis of the immune and bone systems. However, the intestinal role of this molecule is unclear. Here, we show that dextran sodium sulfate (DSS)–induced colitis and azoxymethane-DSS–induced intestinal tumors are reduced in Clec4a2–/– mice independent of intestinal microbiota. STAT5 phosphorylation and expression of Csf2 and tight junction genes are enhanced, while Il17a and Cxcl2 is suppressed in the Clec4a2–/– mouse colon, which exhibits reduced infiltration of neutrophils and myeloid-derived suppressor cells. GM-CSF administration ameliorates DSS colitis associated with reduced Il17a and enhanced tight junction gene expression, whereas anti–GM-CSF exacerbates symptoms. Furthermore, anti-NA2, a ligand for DCIR, ameliorates colitis and prevents colorectal tumors. These observations indicate that blocking DCIR signaling ameliorates colitis and suppresses colonic tumors, suggesting DCIR as a possible target for the treatment of these diseases
2025-07-03 | GSE207631 | GEO
Project description:Ulcerative colitis (UC), belonging to inflammatory bowel disease (IBD), is a chronic and relapsing inflammatory disorders of the gastrointestinal tract, which is not completely cured so far. Valeriana jatamansi is a Chinese medicine used clinically to treat "diarrhea", which is closely related to UC. This study was to elucidate the therapeutic effects of V. jatamansi extract (VJE) on dextran sodium sulfate (DSS)-induced UC in mice and its underlying mechanism. In this work, VJE effectively ameliorate the symptoms, histopathological scores and reduce the production of inflammatory factors of UC mice. The colon untargeted metabolomics analysis and 16S rDNA sequencing showed remarkable differences in colon metabolite profiles and intestinal microbiome composition between the control and DSS groups, and VJE intervention can reduce these differences. Thirty-two biomarkers were found and modulated the primary pathways including pyrimidine metabolism, arginine biosynthesis and glutathione metabolism. Meanwhile, twelve significant taxa of gut microbiota were found. Moreover, there is a close relationship between endogenous metabolites and intestinal flora. These findings suggested that VJE ameliorates UC by inhibiting inflammatory factors, recovering intestinal maladjustment, and regulating the interaction between intestinal microbiota and host metabolites. Therefore, the intervention of V. jatamansi is a potential therapeutic treatment for UC.
2023-07-24 | PXD043047 | Pride
Project description:Intestinal epithelial homeostasis is maintained by a complex interplay between different epithelial cells, gut microorganisms, and immune cells. Disruption of this interplay contributes to inflammatory and immune diseases associated with gut microbiome dysbiosis. A genetic factor that modulates the interactions between gut epithelium, microbiota and immune cells is sirtuin 1 (SIRT1), the most conserved mammalian NAD+-dependent protein deacetylase. We and others have shown that deficiency of intestinal epithelial SIRT1 leads to intestinal inflammation, disruption of gut microbial composition, and altered susceptibility to environmentally induced colitis. Recently we generated a Paneth-cell specific SIRT1 KO mouse model (SIRT1 PKO). Similar to mice with SIRT1 deficiency in whole intestinal epithelium, SIRT1 PKO mice had increased abundance as well as hyperactivation of Paneth cells in vivo and in cultured intestinal organoids. Single-cell RNA-seq of whole intestinal cell populations confirmed that deletion of Paneth cell SIRT1 significantly increases the abundance of Paneth cells. This increase was accompanied with an elevated abundance of intestinal stem cells, transition amplifying cells, and enterocytes. Consistently, SIRT1 PKO mice were able to better maintain their intestinal epithelial integrity during aging and were protected from chemically induced colitis compared to control mice. Deletion of SIRT1 in Paneth cells further induced profound alterations in gut microbiota. Using microbiota-depleted mice and fecal transplantation, we demonstrate that Paneth cell SIRT1 deficiency ameliorates colitis through the gut microbiota. Collectively, our findings uncover an unanticipated function of Paneth cell SIRT1 in conferring sensitivity of the gut epithelium to stress.
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Project description:Extracellular adenosine triphosphate (ATP) released by mucosal immune cells and by microbiota in the intestinal lumen elicits diverse immune responses that mediate the intestinal homeostasis via P2 purinergic receptors, while overactivation of the ATP signaling leads to disruption of mucosal immune system linked to pathogenesis of intestinal inflammation. In the small intestine, hydrolysis of luminal ATP by E-NTPD7 in epithelial cells is essential for control of the number of Th17 cells. However, the molecular mechanism underlying regulation of microbiota-derived ATP in the colon is poorly understood. Here, we show that E-NTPD8 is highly expressed in large intestinal epithelial cells and hydrolyzes microbiota-derived luminal ATP. Compared to wild-type mice, Entpd8-/- mice develop more severe DSS-induced colitis. In this context, either depletion of neutrophils and monocytes by injecting with anti-Gr-1 antibody or introduction of P2rx4 deficiency into hematopoietic cells ameliorates colitis in Entpd8-/- mice. Increased level of luminal ATP in the colon of Entpd8-/- mice promotes glycolysis in neutrophils and monocytes through P2X4 receptor-dependent Ca2+ influx, which links to prolonged survival and elevated ROS production in these cells. Together, these results indicate that E-NTPD8 limits intestinal inflammation by controlling metabolic alteration toward glycolysis via P2X4 receptor in myeloid cells.
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Project description:Extracellular adenosine triphosphate (ATP) released by mucosal immune cells and by microbiota in the intestinal lumen elicits diverse immune responses that mediate the intestinal homeostasis via P2 purinergic receptors, while overactivation of the ATP signaling leads to disruption of mucosal immune system linked to pathogenesis of intestinal inflammation. In the small intestine, hydrolysis of luminal ATP by E-NTPD7 in epithelial cells is essential for control of the number of Th17 cells. However, the molecular mechanism underlying regulation of microbiota-derived ATP in the colon is poorly understood. Here, we show that E-NTPD8 is highly expressed in large intestinal epithelial cells and hydrolyzes microbiota-derived luminal ATP. Compared to wild-type mice, Entpd8-/- mice develop more severe DSS-induced colitis. In this context, either depletion of neutrophils and monocytes by injecting with anti-Gr-1 antibody or introduction of P2rx4 deficiency into hematopoietic cells ameliorates colitis in Entpd8-/- mice. Increased level of luminal ATP in the colon of Entpd8-/- mice promotes glycolysis in neutrophils and monocytes through P2X4 receptor-dependent Ca2+ influx, which links to prolonged survival and elevated ROS production in these cells. Together, these results indicate that E-NTPD8 limits intestinal inflammation by controlling metabolic alteration toward glycolysis via P2X4 receptor in myeloid cells.
2021-09-23 | GSE160380 | GEO
Project description:Extracellular adenosine triphosphate (ATP) released by mucosal immune cells and by microbiota in the intestinal lumen elicits diverse immune responses that mediate the intestinal homeostasis via P2 purinergic receptors, while overactivation of the ATP signaling leads to disruption of mucosal immune system linked to pathogenesis of intestinal inflammation. In the small intestine, hydrolysis of luminal ATP by E-NTPD7 in epithelial cells is essential for control of the number of Th17 cells. However, the molecular mechanism underlying regulation of microbiota-derived ATP in the colon is poorly understood. Here, we show that E-NTPD8 is highly expressed in large intestinal epithelial cells and hydrolyzes microbiota-derived luminal ATP. Compared to wild-type mice, Entpd8-/- mice develop more severe DSS-induced colitis. In this context, either depletion of neutrophils and monocytes by injecting with anti-Gr-1 antibody or introduction of P2rx4 deficiency into hematopoietic cells ameliorates colitis in Entpd8-/- mice. Increased level of luminal ATP in the colon of Entpd8-/- mice promotes glycolysis in neutrophils and monocytes through P2X4 receptor-dependent Ca2+ influx, which links to prolonged survival and elevated ROS production in these cells. Together, these results indicate that E-NTPD8 limits intestinal inflammation by controlling metabolic alteration toward glycolysis via P2X4 receptor in myeloid cells.
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Project description:In human volunteers, we evaluated changes in gene expression profiles, immunological indices, and intestinal microbiota of blood cells in subjects consuming a S.reticulata extract. Thirty healthy Japanese males were split randomly into a group ingesting 240 mg/day of S.reticulata extract -containing tablets for 4 weeks and a control group ingesting placebo tablets. Ingestion of the S.reticulata extract improved T cell proliferation and other immunological indices, and changed intestinal microbiota, increasing Bifidobacterium and Lactobacillales and decreasing Clostridium bacteria. Expression levels of many immuno-relevant genes were altered. We have shown the S.reticulata extract to enhance human immune functions.
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Project description:The goal of this project is to find out whether human intestinal IgA1 and IgA2 secretion, transport and reactivity towards the microbiota might be involved in dysbiosis induction during Crohn’s disease and Ulcerative colitis. Mass spectrometry was used to characterize SIgA from Crohn’s disease patient and Ulcerative colitis patient, in term of O- and N-glycosylation in order to study their reverse transcytosis capacity and their role in intestinal inflammation.
2022-06-27 | PXD024060 | Pride
Project description:Intestinal microbial dysbiosis is associated with Crohn’s disease (CD). However, the mechanisms leading to the chronic mucosal inflammation that characterizes this disease remain unclear. To evaluate causality and mechanisms of disease, we conducted a systems level study of the interactions between the gut microbiota and host in new-onset pediatric patients. We report an altered host proteome in CD patients indicative of impaired mitochondrial functions. A downregulation of mitochondrial proteins implicated in H2S detoxification was observed, while the relative abundance of H2S microbial producers was increased. Network correlation analysis identified Atopobium parvulum as the central hub of H2S producers. Gnotobiotic and conventionalized colitis-susceptible interleukin-10-deficient (Il10-/-) mice demonstrated that A. parvulum induced colitis, a phenotype requiring the presence of the intestinal microbiota. Administration of bismuth, a H2S scavenger, prevented A. parvulum-induced colitis in Il10-/- mice. This study identified host-microbiota interactions that are disturbed in CD patients providing mechanistic insights on CD pathogenesis.
2016-09-29 | PXD002882 | Pride
Project description:Background & Aims: The complex interactions between diet and the microbiota that influence mucosal inflammation and inflammatory bowel disease are poorly understood. Experimental colitis models provide the opportunity to control and systematically perturb diet and the microbiota in parallel to quantify the contributions between multiple dietary ingredients and the microbiota on host physiology and colitis. Methods: To examine the interplay of diet and the gut microbiota on host health and colitis, we fed over 40 different diets with varied macronutrient sources and concentrations to specific pathogen free or germ free mice either in the context of healthy, unchallenged animals or dextran sodium sulfate colitis model. Results: Diet influenced physiology in both health and colitis across all models, with the concentration of protein and psyllium fiber having the most profound effects. Increasing dietary protein elevated gut microbial density and worsened DSS colitis severity. Depleting gut microbial density by using germ-free animals or antibiotics negated the effect of a high protein diet. Psyllium fiber influenced host physiology and attenuated colitis severity through microbiota-dependent and microbiota-independent mechanisms. Combinatorial perturbations to dietary protein and psyllium fiber in parallel explain most variation in gut microbial density, intestinal permeability, and DSS colitis severity, and changes in one ingredient can be offset by changes in the other. Conclusions: Our results demonstrate the importance of examining complex mixtures of nutrients to understand the role of diet in intestinal inflammation. Keywords: IBD; Diet; Microbiota; Mouse Models; Systems Biology
2017-10-30 | GSE104461 | GEO