Ontology highlight
ABSTRACT:
PROVIDER: PRJNA891885 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22034100.fastq.gz | Fastqsanger.gz | |||
| SRR22034101.fastq.gz | Fastqsanger.gz | |||
| SRR22034102.fastq.gz | Fastqsanger.gz | |||
| SRR22034103.fastq.gz | Fastqsanger.gz | |||
| SRR22034104.fastq.gz | Fastqsanger.gz |
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Project description:Background and Aims. Dendritic cells (DCs) play a pivotal role in maintaining immunological homeostasis by orchestrating innate and adaptive immune responses via migration to inflamed sites and the lymph nodes (LNs). Plasmacytoid DCs (pDCs) have been reported to accumulate in the colon of inflammatory bowel disease (IBD) patients and dextran sulfate sodium (DSS)-induced colitis mice. However, the role of pDCs in the progression of colonic inflammation remains unclear. Methods. 80 compounds in natural medicines were searched for inhibitors of pDC migration using bone marrow-derived pDCs (BMpDCs) and conventional DCs (BMcDCs). BALB/c mice were given 3% DSS in the drinking water for 7 days to induce acute colitis. Compounds, which specifically inhibited pDC migration, were administrated into DSS-induced colitis mice. Results. Astragaloside IV (As-IV) and oxymatrine (Oxy) suppressed BMpDC migration but not BMcDC migration. In DSS-induced colitis mice, the number of pDCs was markedly increased in the colonic lamina propria (LP), and the expression of CCL21 was obviously observed in colonic isolated lymphoid follicles (ILFs). As-IV and Oxy reduced symptoms of colitis and the accumulation of pDCs in colonic ILFs but not in the colonic LP. Moreover, in a BMpDC adoptive transfer model, BMpDC migration to colonic ILFs was significantly decreased by treatment with As-IV or Oxy. Conclusion. pDCs accumulated in the colon of DSS-induced colitis mice, and As-IV and Oxy ameliorated DSS-induced colitis by suppressing pDC migration to colonic ILFs. Accordingly, the selective inhibition of pDC migration may be a potential therapeutic approach for treating colonic inflammatory diseases.
2021-07-06 | GSE167388 | GEO
Project description:The gut microbiome consists of a multi-kingdom microbial community. Whilst the role of bacteria as causal contributors governing host physiological development is well established, the role of fungi remains to be determined. Here, we use germ-free mice colonized with defined species of bacteria, fungi, or both to differentiate the causal role of fungi on microbiome assembly, immune development, susceptibility to colitis, and airway inflammation. Fungal colonization promotes major shifts in bacterial microbiome ecology, and has an independent effect on innate and adaptive immune development in young mice. While exclusive fungal colonization is insufficient to elicit overt dextran sulfate sodium-induced colitis, bacterial and fungal co-colonization increase colonic inflammation. Ovalbumin-induced airway inflammation reveals that bacterial, but not fungal colonization is necessary to decrease airway inflammation, yet fungi selectively promotes macrophage infiltration in the airway. Together, our findings demonstrate a causal role for fungi in microbial ecology and host immune functionality, and therefore prompt the inclusion of fungi in therapeutic approaches aimed at modulating early life microbiomes.
2022-01-14 | MTBLS1679 | MetaboLights
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:immune cells in intestinal lamina propria play important roles in pathogenesis of DSS colitis. Here, we used single cell RNA sequencing (scRNA-seq) to reveale the intestinal immune landscape of DSS colitis and study the effects of Ring1A on intestinal immune cells.
2023-09-13 | GSE210866 | GEO
Project description:Purpose: Gut microbiota-derived metabolites play a pivotal role in the maintenance of local gut homeostasis and can even induce systemic effects via accumulation in the bloodstream. Here, we demonstrate that mono-colonization of germ-free (GF) mice with Clostridium sporogenes protects mice from inflamation and death induced by DSS colitis. Method: 8-12-week-old male mice (GF, SPF and GF colonized with C. sporogenes (CS)) were treated with 2.5% DSS in drinking water for 5 days and colon tissue was isolated on day 7. RNA was isolated from the colon tissue and RNA sequenzing was performed. Results: Mono-colonization of GF mice with Clostridium sporogenes protected the mice from DSS colitis induced death, while producing high amounts of indole-3-propionic acid (IPA), branched chain (BCFA) and short-chain (SCFA) fatty acids. In comparison to CS mice, SPF mice showed much higher levels of inflammatory related genes and a worse histological score. Conclusion: Histological stainings and the RNAseq both showed high levels of protection of C. sporogenes colonized mice in colitis, compared to SPF and GF animals. The data provide evidence for a therapeutic potential of C. sporogenes for IBD patients.
2024-10-15 | GSE264024 | GEO
Project description:<p>Cecal contents metabolomics analysis of DSS-induced colitis mice and DSS-induced colitis mice with V. parvula colonization.</p>
2025-08-12 | MTBLS12276 | MetaboLights
Project description:Dextran sulfate sodium (DSS)-induced colitis is a widely used model to study ulcerative colitis (UC). However, the extent to which acute versus repeated DSS exposure mimics human disease remains unclear. Using histopathology, flow cytometry, single-cell RNA sequencing (scRNA-seq) and 16S rRNA profiling we compared disease outcomes, immune infiltrate, transcriptional programs and changes in the microbiome in mice subjected to a single (acute) versus two (repeated) DSS cycles. We found that repeated cycles of DSS-induced colitis in mice result in more severe intestinal inflammation compared to a single exposure, with increased PMN and T cell infiltration, mucosal remodeling, and microbiota normalization. Single-cell transcriptomics revealed that acute vs repeated DSS exposure drives differential programs in immune cell subtypes distinctly overlapping with human UC. Overall, our findings suggest that repeated DSS exposure may more accurately models human disease, highlighting its utility for translational IBD research.
2025-10-31 | GSE306845 | GEO
Project description:IL17B protected mice from dextran sodium sulfate (DSS)-induced colitis since IL17B deficiency resulted in severe DSS-induced colitis with exaggerated weight loss, shorter colon length, and elevated proinflammatory cytokine production in colon. For mechanism study, we use single cell transcriptional analyses of CD45+ immune cells in colonic lamina propria to detect the effect of IL-17B on colon LP immune cells in colitis. We found increased inflammatory macrophages infiltration in colon lamina propria after colitis induction expressing inflammatory cytokines such as S100a9, S100a8, Tnf, which was confirmed by real-time PCR and flow cytometry. Reconstitute of Il17b-/- mice with recombinant IL17B alleviated the severity of DSS-induced colitis. IL17B treatment also inhibited LPS-induced inflammation in bone marrow derived macrophage and in mice. These data indicate that IL17B exerting its inhibitory role in inflammation by regulating inflammatory macrophage response. In view of the protective effect of IL17B on DSS-induced colitis and LPS-induced inflammation, IL17B might represent a novel potential therapeutic approach to treat the inflammation.
2023-01-17 | GSE161987 | GEO