Effect of FcεRIα Deficiency on gene expression of gut epithial cell
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE254286 | GEO | 2024/10/08
REPOSITORIES: GEO
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Project description:Gut dysbiosis is closely involved in the pathogenesis of inflammatory bowel disease (IBD). However, it remains unclear whether IBD-associated gut dysbiosis plays a primary role in disease manifestation or is merely secondary to intestinal inflammation. Here, we established a humanized gnotobiotic (hGB) mouse system to assess the functional role of gut dysbiosis associated with two types of IBD - Crohn's disease (CD) and ulcerative colitis (UC). In order to explore the functional impact of dysbiotic microbiota in IBD patients on host immune responses, we analyzed gene expression profiles in colonic mucosa of hGB mice colonized with healty (HC), CD, and UC microbiota.
2015-10-10 | GSE73882 | GEO
Project description:Abstract. Background: The cause of ulcerative colitis (UC) is not yet fully understood. Previous research has pointed towards a potential role for mutations in NOD2 in promoting the onset and progression of inflammatory bowel disease (IBD) by altering the microbiota of the gut. However, the relationship between toll-like receptor 4 (TLR4) and gut microbiota in IBD is not well understood. To shed light on this, the interaction between TLR4 and gut microbiota was studied using a mouse model of IBD. Methods: To examine the function of TLR4 signaling in intestinal injury repair, researchers developed Dextran Sulfate Sodium Salt (DSS)-induced colitis and injury models in both wild-type (WT) mice and TLR4 knockout (TLR4-KO) mice. To assess changes in the gut microbiota, 16S rRNA sequencing was conducted on fecal samples from both the TLR4-KO and WT enteritis mouse models. Results: The data obtained depicted a protective function of TLR4 against DSS-induced colitis. The gut microbiota composition was found to vary considerably between the WT and TLR4-KO mice groups as indicated by β-diversity analysis and operational taxonomic units (OTUs) cluster. Statistical analysis of microbial multivariate variables depicted an elevated abundance of Escherichia coli/Shigella, Gammaproteobacteria, Tenerlcutes, Deferribacteres, Enterobacteria, Rikenellaceae, and Proteobacteria in the gut microbiota of TLR4-KO mice, whereas there was a considerable reduction in Bacteroidetes at five different levels of the phylogenetic hierarchy including phylum, class, order, family, and genus in comparison with the WT control. Conclusion: TLR4 may protect intestinal epithelial cells from damage in response to DSS-induced injury by controlling the microbiota in the gut.
2023-11-01 | GSE227565 | GEO
Project description:Triclosan (TCS), an antimicrobial agent in thousands of consumer products, is a risk factor for colitis and colitis-associated colorectal cancer. While the intestinal toxicities of TCS require the presence of gut microbiota, the molecular mechanisms involved have not been defined. Here we show that intestinal commensal microbes mediate metabolic activation of TCS in the colon and drive its gut toxicology. Using a range of in vitro, ex vivo, and in vivo approaches, we identify specific microbial β-glucuronidase (GUS) enzymes involved and pinpoint molecular motifs required to metabolically activate TCS in the gut. Finally, we show that targeted inhibition of bacterial GUS enzymes abolishes the colitis-promoting effects of TCS, supporting the essential roles of specific microbial proteins in TCS toxicity. Our results define a mechanism by which intestinal microbes cause the gut toxicity of environmental chemicals and suggest a therapeutic approach to alleviate colitis and associated diseases.
2021-11-04 | PXD025887 | Pride
Project description:We show that oxidized LA, rather than LA itself,exacerbates colitis via Toll-like receptor 4 (TLR4)- and gut microbiota-dependent mechanisms.Administration of a diet containing oxidized LA, at low human-consumption levels, increases the severity of colitis and exacerbates the development of colorectal tumorigenesis in mice.
2023-12-31 | GSE209580 | GEO
Project description:Background & Aims: Gut microbiota dysbiosis is associated with the pathogenesis of Crohn's disease (CD), but the underlying mechanisms by which colon bacteria contribute to the development of CD remain largely unclear. Here, we investigated whether colon bacteria, particularly Bacteroides acidifaciens (B. acidifaciens), promote CD pathogenesis through their small RNAs (sRNAs). Methods: The composition of gut bacteria were analyzed in the fecal samples of IL-10 knockout (KO) mice and CD45RBhigh mice that spontaneously develop colitis via 16S amplification sequencing, and the expression pattern of B. acidifaciens in both experimental colitis mice and CD patients was confirmed by quantitative RT-PCR (qRT-PCR). The effects of B. acidifaciens and their total and small RNA contents on colitis development were evaluated in IL-10 KO mice. Furthermore, the expression profile of B. acidifaciens-derived sRNA (BA-sRNA) in IL-10 KO mice was established by RNA sequencing, and BA-sRNA-172 levels in experimental colitis mice and CD patients were determined. Lentivirus carrying BA-sRNA-172 and BA-sRNA-172-deficient B. acidifaciens were then constructed and used to investigate the role of BA-sRNA-172 in the development of colitis. The activities of BA-sRNA-172 in regulating mucin2 (MUC2) expression and gut mucosal barrier function was systematically studied by in situ hybridization, immunofluorescence staining, qRT-PCR, western blot, RNA pull-down and luciferase assays in vitro. Finally, the effects of anti-BA-sRNA-172 and anti-MUC2 shRNA on intestinal barrier function and colitis development were evaluated. Results: Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (build mm9) and identified 16,014 transcripts in the retinas of WT and Nrl−/− mice with BWA workflow and 34,115 transcripts with TopHat workflow. RNA-seq data confirmed stable expression of 25 known housekeeping genes, and 12 of these were validated with qRT–PCR. RNA-seq data had a linear relationship with qRT–PCR for more than four orders of magnitude and a goodness of fit (R2) of 0.8798. Approximately 10% of the transcripts showed differential expression between the WT and Nrl−/− retina, with a fold change ≥1.5 and p value <0.05. Altered expression of 25 genes was confirmed with qRT–PCR, demonstrating the high degree of sensitivity of the RNA-seq method. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to retinal function. Data analysis with BWA and TopHat workflows revealed a significant overlap yet provided complementary insights in transcriptome profiling. Conclusions: Our study represents the first detailed analysis of retinal transcriptomes, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a cell or tissue. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.
2023-08-13 | GSE155040 | GEO
Project description:Purpose: To study the differential expression of gut bacterial mRNAs during chronic organophosphate treatment. Methods: Balb/c mice were treated with organophosphate (monocrotophos 28 ug/kg body weight/day) directly in drinking water for 180 days. Glucose tolerance tests indicated the induction of glucose intolerance. The total RNA was isolated by using TRIZOL from the cecal tissue that is cleared off fecal contents and subsequently the eukaryotic and bacterial rRNAs were removed by using MicrobExpress and MicrobEnrich kits (Ambion). Subsequently, RNA library was contructed using illumina kit as per manufacturer's instructions. Results: The reads were annotated to the reference human gut microbiome database and we found differential expression of large number of genes especially those involved in organophosphate degradation. Our subsequent studies proved that gut microbial degradation of organophosphates induces glucose intolerance via gluconeogenesis. Conclusions: Chronic organophosphate-induced hyperglycemia is mediated by the organosphosphate-degrading potential of gut microbiota.
2016-12-07 | GSE90843 | GEO
Project description:Background & Aims: Gut microbiota dysbiosis is associated with the pathogenesis of Crohn's disease (CD), but the underlying mechanisms by which colon bacteria contribute to the development of CD remain largely unclear. Here, we investigated whether colon bacteria, particularly Bacteroides acidifaciens (B. acidifaciens), promote CD pathogenesis through their small RNAs (sRNAs). Methods: The composition of gut bacteria were analyzed in the fecal samples of IL-10 knockout (KO) mice and CD45RBhigh mice that spontaneously develop colitis via 16S amplification sequencing, and the expression pattern of B. acidifaciens in both experimental colitis mice and CD patients was confirmed by quantitative RT-PCR (qRT-PCR). The effects of B. acidifaciens and their total and small RNA contents on colitis development were evaluated in IL-10 KO mice. Furthermore, the expression profile of B. acidifaciens-derived sRNA (BA-sRNA) in IL-10 KO mice was established by RNA sequencing, and BA-sRNA-172 levels in experimental colitis mice and CD patients were determined. Lentivirus carrying BA-sRNA-172 and BA-sRNA-172-deficient B. acidifaciens were then constructed and used to investigate the role of BA-sRNA-172 in the development of colitis. The activities of BA-sRNA-172 in regulating mucin2 (MUC2) expression and gut mucosal barrier function was systematically studied by in situ hybridization, immunofluorescence staining, qRT-PCR, western blot, RNA pull-down and luciferase assays in vitro. Finally, the effects of anti-BA-sRNA-172 and anti-MUC2 shRNA on intestinal barrier function and colitis development were evaluated. Results: Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (build mm9) and identified 16,014 transcripts in the retinas of WT and Nrl−/− mice with BWA workflow and 34,115 transcripts with TopHat workflow. RNA-seq data confirmed stable expression of 25 known housekeeping genes, and 12 of these were validated with qRT–PCR. RNA-seq data had a linear relationship with qRT–PCR for more than four orders of magnitude and a goodness of fit (R2) of 0.8798. Approximately 10% of the transcripts showed differential expression between the WT and Nrl−/− retina, with a fold change ≥1.5 and p value <0.05. Altered expression of 25 genes was confirmed with qRT–PCR, demonstrating the high degree of sensitivity of the RNA-seq method. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to retinal function. Data analysis with BWA and TopHat workflows revealed a significant overlap yet provided complementary insights in transcriptome profiling. Conclusions: Our study represents the first detailed analysis of retinal transcriptomes, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a cell or tissue. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.
2023-08-13 | GSE155039 | GEO
Project description:Background & Aims: Gut microbiota dysbiosis is associated with the pathogenesis of Crohn's disease (CD), but the underlying mechanisms by which colon bacteria contribute to the development of CD remain largely unclear. Here, we investigated whether colon bacteria, particularly Bacteroides acidifaciens (B. acidifaciens), promote CD pathogenesis through their small RNAs (sRNAs). Methods: The composition of gut bacteria were analyzed in the fecal samples of IL-10 knockout (KO) mice and CD45RBhigh mice that spontaneously develop colitis via 16S amplification sequencing, and the expression pattern of B. acidifaciens in both experimental colitis mice and CD patients was confirmed by quantitative RT-PCR (qRT-PCR). The effects of B. acidifaciens and their total and small RNA contents on colitis development were evaluated in IL-10 KO mice. Furthermore, the expression profile of B. acidifaciens-derived sRNA (BA-sRNA) in IL-10 KO mice was established by RNA sequencing, and BA-sRNA-172 levels in experimental colitis mice and CD patients were determined. Lentivirus carrying BA-sRNA-172 and BA-sRNA-172-deficient B. acidifaciens were then constructed and used to investigate the role of BA-sRNA-172 in the development of colitis. The activities of BA-sRNA-172 in regulating mucin2 (MUC2) expression and gut mucosal barrier function was systematically studied by in situ hybridization, immunofluorescence staining, qRT-PCR, western blot, RNA pull-down and luciferase assays in vitro. Finally, the effects of anti-BA-sRNA-172 and anti-MUC2 shRNA on intestinal barrier function and colitis development were evaluated. Results: Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (build mm9) and identified 16,014 transcripts in the retinas of WT and Nrl−/− mice with BWA workflow and 34,115 transcripts with TopHat workflow. RNA-seq data confirmed stable expression of 25 known housekeeping genes, and 12 of these were validated with qRT–PCR. RNA-seq data had a linear relationship with qRT–PCR for more than four orders of magnitude and a goodness of fit (R2) of 0.8798. Approximately 10% of the transcripts showed differential expression between the WT and Nrl−/− retina, with a fold change ≥1.5 and p value <0.05. Altered expression of 25 genes was confirmed with qRT–PCR, demonstrating the high degree of sensitivity of the RNA-seq method. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to retinal function. Data analysis with BWA and TopHat workflows revealed a significant overlap yet provided complementary insights in transcriptome profiling. Conclusions: Our study represents the first detailed analysis of retinal transcriptomes, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a cell or tissue. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.
2023-08-13 | GSE155038 | GEO
Project description:Background & Aims: Gut microbiota dysbiosis is associated with the pathogenesis of Crohn's disease (CD), but the underlying mechanisms by which colon bacteria contribute to the development of CD remain largely unclear. Here, we investigated whether colon bacteria, particularly Bacteroides acidifaciens (B. acidifaciens), promote CD pathogenesis through their small RNAs (sRNAs). Methods: The composition of gut bacteria were analyzed in the fecal samples of IL-10 knockout (KO) mice and CD45RBhigh mice that spontaneously develop colitis via 16S amplification sequencing, and the expression pattern of B. acidifaciens in both experimental colitis mice and CD patients was confirmed by quantitative RT-PCR (qRT-PCR). The effects of B. acidifaciens and their total and small RNA contents on colitis development were evaluated in IL-10 KO mice. Furthermore, the expression profile of B. acidifaciens-derived sRNA (BA-sRNA) in IL-10 KO mice was established by RNA sequencing, and BA-sRNA-172 levels in experimental colitis mice and CD patients were determined. Lentivirus carrying BA-sRNA-172 and BA-sRNA-172-deficient B. acidifaciens were then constructed and used to investigate the role of BA-sRNA-172 in the development of colitis. The activities of BA-sRNA-172 in regulating mucin2 (MUC2) expression and gut mucosal barrier function was systematically studied by in situ hybridization, immunofluorescence staining, qRT-PCR, western blot, RNA pull-down and luciferase assays in vitro. Finally, the effects of anti-BA-sRNA-172 and anti-MUC2 shRNA on intestinal barrier function and colitis development were evaluated. Results: Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (build mm9) and identified 16,014 transcripts in the retinas of WT and Nrl−/− mice with BWA workflow and 34,115 transcripts with TopHat workflow. RNA-seq data confirmed stable expression of 25 known housekeeping genes, and 12 of these were validated with qRT–PCR. RNA-seq data had a linear relationship with qRT–PCR for more than four orders of magnitude and a goodness of fit (R2) of 0.8798. Approximately 10% of the transcripts showed differential expression between the WT and Nrl−/− retina, with a fold change ≥1.5 and p value <0.05. Altered expression of 25 genes was confirmed with qRT–PCR, demonstrating the high degree of sensitivity of the RNA-seq method. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to retinal function. Data analysis with BWA and TopHat workflows revealed a significant overlap yet provided complementary insights in transcriptome profiling. Conclusions: Our study represents the first detailed analysis of retinal transcriptomes, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a cell or tissue. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.
2023-08-13 | GSE155035 | GEO
Project description:Interleukin-10 (IL-10) is a pleiotropic anti-inflammatory cytokine produced and sensed by most hematopoietic cells. Genome wide association studies and experimental animal models point at a central role of the IL-10 axis in Inflammatory Bowel Diseases. Here we investigated the importance of intestinal macrophage production of IL-10 and their IL-10 exposure, as well as the existence of an IL-10-based autocrine regulatory loop in the gut. Specifically, we generated mice harboring IL-10 or IL-10 receptor (IL-10R?) mutations in intestinal lamina propria-resident chemokine receptor CX3CR1hi-expressingmacrophages. We found macrophage-derived IL-10 dispensable for gut homeostasis and maintenance of colonic T regulatory cells. In contrast, loss of IL-10 receptor expression impaired the critical conditioning of these monocyte-derived macrophages, but resulted in spontaneous development of severe colitis. Collectively, our results highlight IL-10 as a critical homeostatic macrophage-conditioning factor in the colon and define intestinal CX3CR1hi macrophages as a decisive factor that determines gut health or inflammation. Microarray of resident macrophages sorted from colons of Interleukin-10 deficeint mice and macrophage-restricted interleukin-10 receptor deficient mice versus colonic resident macrophages of wild type mice
2014-05-09 | E-GEOD-56444 | biostudies-arrayexpress