Ontology highlight
ABSTRACT:
PROVIDER: PRJNA703330 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13753900_1.fastq.gz | Fastqsanger.gz | |||
| SRR13753900_2.fastq.gz | Fastqsanger.gz | |||
| SRR13753901_1.fastq.gz | Fastqsanger.gz | |||
| SRR13753901_2.fastq.gz | Fastqsanger.gz | |||
| SRR13753902_1.fastq.gz | Fastqsanger.gz |
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Project description:Objective: Inflammatory bowel disease (IBD), encompassing ulcerative colitis (UC) and Crohn’s disease (CD), represents a challenging group of chronic gastrointestinal inflammatory disorders. While trained immunity, a form of innate immune memory, has shown promise in combating infection and cancer, its role in chronic inflammatory diseases, particularly inflammatory bowel disease (IBD), remains relatively underexplored. This study aims to investigate the potential of trained immunity to ameliorate IBD. Results: BG induced trained immunity significantly ameliorates DSS-induced colitis. Mechanistically, β-glucan primed the hematopoietic compartment, leading to a profound shift in monocyte fuction. Both bone marrow transplantation from trained donors to naïve recipients and adoptive transfer of trained peripheral monocytes provided protection against DSS colitis. Notably, trained mice displayed enhanced bactericidal activity against intestinal bacterial infections. Furthermore, single-cell RNA sequencing revealed that β-glucan-induced trained immunity resulted in an expansion of reparative Cx3cr1 intestinal macrophages originating from Ly6Chi monocytes, facilitating faster recovery of the colon epithelium. Conclusion: Our findings demonstrate that β-glucan effectively induces trained immunity, leading to a multifaceted protective response against experimental colitis. These findings provide compelling evidence for the therapeutic potential of harnessing trained immunity to treat IBD and offer a novel approach to modulating intestinal inflammation and restoring gut homeostasis.
2026-01-01 | GSE285860 | GEO
Project description:Objective: Inflammatory bowel disease (IBD), encompassing ulcerative colitis (UC) and Crohn’s disease (CD), represents a challenging group of chronic gastrointestinal inflammatory disorders. While trained immunity, a form of innate immune memory, has shown promise in combating infection and cancer, its role in chronic inflammatory diseases, particularly inflammatory bowel disease (IBD), remains relatively underexplored. This study aims to investigate the potential of trained immunity to ameliorate IBD. Results: BG induced trained immunity significantly ameliorates DSS-induced colitis. Mechanistically, β-glucan primed the hematopoietic compartment, leading to a profound shift in monocyte fuction. Both bone marrow transplantation from trained donors to naïve recipients and adoptive transfer of trained peripheral monocytes provided protection against DSS colitis. Notably, trained mice displayed enhanced bactericidal activity against intestinal bacterial infections. Furthermore, single-cell RNA sequencing revealed that β-glucan-induced trained immunity resulted in an expansion of reparative Cx3cr1 intestinal macrophages originating from Ly6Chi monocytes, facilitating faster recovery of the colon epithelium. Conclusion: Our findings demonstrate that β-glucan effectively induces trained immunity, leading to a multifaceted protective response against experimental colitis. These findings provide compelling evidence for the therapeutic potential of harnessing trained immunity to treat IBD and offer a novel approach to modulating intestinal inflammation and restoring gut homeostasis。
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Project description:The use of lenvatinib (Lenv) in advanced hepatocellular carcinoma (HCC) patients is associated with a range of adverse events, including gastrointestinal toxicities, yet the underlying mechanisms remain poorly understood. Here, we demonstrated that Lenv exacerbated both acute and chronic colitis in mouse models by impairing intestinal B cell homeostasis, leading to reduce intestinal B cells and plasma cells, along with decreased IL-10 and IgA secretion. Mechanistically, Lenv decreased MAdCAM-1 expression in intestinal vascular endothelial cells via the VEGFR/PLCγ/PKC/p65 signaling, thereby disrupting B cell homing to the gut. Notably, blockade of either p65 or MAdCAM-1 abrogated Lenv-induced B cell loss and colitis exacerbation. Furthermore, in both tumor-bearing mice and HCC patients receiving Lenv treatment, decreased serum sMAdCAM-1 levels correlated with reduced serum IgA and disruption of intestinal immune homeostasis. Thus, our results show a mechanism for Lenv disrupts intestinal immune homeostasis and implicate serum sMAdCAM-1 may serve as a potential biomarker for monitoring B cell-mediated intestinal immune dysfunction during Lenv therapy.
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Project description:The use of lenvatinib (Lenv) in advanced hepatocellular carcinoma (HCC) patients is associated with a range of adverse events, including gastrointestinal toxicities, yet the underlying mechanisms remain poorly understood. Here, we demonstrated that Lenv exacerbated both acute and chronic colitis in mouse models by impairing intestinal B cell homeostasis, leading to reduce intestinal B cells and plasma cells, along with decreased IL-10 and IgA secretion. Mechanistically, Lenv decreased MAdCAM-1 expression in intestinal vascular endothelial cells via the VEGFR/PLCγ/PKC/p65 signaling, thereby disrupting B cell homing to the gut. Notably, blockade of either p65 or MAdCAM-1 abrogated Lenv-induced B cell loss and colitis exacerbation. Furthermore, in both tumor-bearing mice and HCC patients receiving Lenv treatment, decreased serum sMAdCAM-1 levels correlated with reduced serum IgA and disruption of intestinal immune homeostasis. Thus, our results show a mechanism for Lenv disrupts intestinal immune homeostasis and implicate serum sMAdCAM-1 may serve as a potential biomarker for monitoring B cell-mediated intestinal immune dysfunction during Lenv therapy.
2026-04-11 | GSE327044 | GEO
Project description:BACKGROUND & AIMS: Inflammatory Bowel Disease (IBD) is a chronic inflammatory condition driven by loss of homeostasis between the mucosal immune system, the commensal gut microbiota, and the intestinal epithelium. Our overarching goal is to understand how these components of the intestinal ecosystem cooperate to control homeostasis and to identify novel signal transduction pathways that become dysregulated in IBD. METHODS: We have applied a multi-scale systems biology approach to a mouse model of chronic colitis. We combined quantitative measures of epithelial hyperplasia and immune infiltration with multivariate analysis of inter- and intra-cellular signaling molecules in order to generate a tissue level model of the inflamed disease state. We utilized the computational model to identify signaling pathways that were dysregulated in the context of colitis and then validated model predictions by measuring the effect of small molecule pathway inhibitors on colitis. RESULTS: Our data-driven computational model identified mTOR signaling as a potential driver of inflammation and mTOR inhibition reversed the molecular, immunological, and epithelial manifestations of colitis. Inhibition of Notch signaling, which induces epithelial differentiation, had the same effect, suggesting that the epithelial proliferation/differentiation state plays a key role in maintaining homeostasis of the colon. Confirming this, we found that colonic organoids grown ex vivo showed a similar relationship between proliferation and cytokine expression, even in the absence of gut bacteria and immune cells. CONCLUSIONS: Our study provides a tissue-level systems biology perspective of murine colitis and suggests that mTOR plays a key role in regulating colonic homeostasis by controlling epithelial proliferation/differentiation state. We used microarrays to examine changes in global gene expression patterns associated with chronic inflammation induced by the T cell transfer model of Inflammatory Bowel Disease.
2018-02-05 | GSE87317 | GEO
Project description:IBD is characterized by chronic recurrences of intestinal inflammation and intestinal immune disturbances.Bacteroides vulgatus can alleviate DSS-induced colitis in mice, but the mechanism is unknown. The aim of this study was to examine the changes in gene expression in the intestinal tissue of mice with colitis following treatment with Bacteroides vulgatus by RNA sequencing.
2023-12-06 | GSE246118 | GEO
Project description:Inflammatory bowel disease (IBD) is a chronic, relapsing, and remitting disease characterized by chronic inflammation in the gastrointestinal tract. The exact etiology and pathogenesis of IBD remain elusive. Although ELF-1 has been known to be highly expressed in epithelial cells for past twenty years, little is known about its function in epithelial cells and epithelial-related IBD. Here, we demonstrated that ELF-1 deficiency in mouse lead to exacerbated DSS-induced colitis, marked by inflammation dominated by neutrophil infiltration and activation of IL-17 signaling pathways in various immune cells, including Th17, ILC3, γδT and NKT cells. Bone marrow transfer experiments confirmed ELF-1 deficiency in non-hematopoietic cells intrinsically worsened DSS-induced colitis. On one hand, ELF-1 deficiency enhanced the production of pro-inflammatory chemokines in colonic epithelial cells, leading to extensive infiltration of neutrophils and other immune cells into the colonic mucosal tissue. On the other hand, ELF-1 directly regulated the expression of the Rack1 gene in colonic epithelial tissue, which has been proved to play critical roles in maintaining intestinal homeostasis. Altogether, ELF-1 plays a protective role in colitis by maintaining intestinal epithelium homeostasis.
2025-02-12 | GSE289183 | GEO
Project description:Histone deacetylases (Hdac) remove acetyl groups from proteins, influencing global and specific gene expression. Hdacs control inflammation, as shown by Hdac inhibitor-dependent protection from DSS-induced murine colitis. While tissue-specific Hdac knockouts show redundant and specific functions, little is known of their intestinal epithelial cell (IEC) role. We have shown previously that dual Hdac1/Hdac2 IEC-specific loss disrupts cell proliferation and determination, with decreased secretory cell numbers and altered barrier function. We thus investigated how compound Hdac1/Hdac2 or Hdac2 IEC-specific deficiency alters the inflammatory response. Floxed Hdac1 and Hdac2 and villin-Cre mice were interbred. Compound Hdac1/Hdac2 IEC-deficient mice showed chronic basal inflammation, with increased basal Disease Activity Index (DAI) and deregulated Reg gene colonic expression. DSS-treated dual Hdac1/Hdac2 IEC-deficient mice displayed increased DAI, histological score, intestinal permeability and inflammatory gene expression. In contrast to double knockouts, Hdac2 IEC-specific loss did not affect IEC determination and growth, nor result in chronic inflammation. However, Hdac2 disruption protected against DSS colitis, as shown by decreased DAI, intestinal permeability and caspase-3 cleavage. Hdac2 IEC-specific deficient mice displayed increased expression of IEC gene subsets, such as colonic antimicrobial Reg3b and Reg3g mRNAs, and decreased expression of immune cell function-related genes. Our data show that Hdac1 and Hdac2 are essential IEC homeostasis regulators. IEC-specific Hdac1 and Hdac2 may act as epigenetic sensors and transmitters of environmental cues and regulate IEC-mediated mucosal homeostatic and inflammatory responses. Different levels of IEC Hdac activity may lead to positive or negative outcomes on intestinal homeostasis during inflammation Total RNAs from the colon of three control and three Hdac2 IEC-specific knockout mice were isolated with the Rneasy kit (Qiagen, Mississauga, ON, Canada).
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