Ontology highlight
ABSTRACT:
PROVIDER: PRJNA925499 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23217323_1.fastq.gz | Fastqsanger.gz | |||
| SRR23217323_2.fastq.gz | Fastqsanger.gz | |||
| SRR23217324_1.fastq.gz | Fastqsanger.gz | |||
| SRR23217324_2.fastq.gz | Fastqsanger.gz | |||
| SRR23217325_1.fastq.gz | Fastqsanger.gz |
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Project description:Epidemiological studies have indicated an association between statin use and reduced incidence of colorectal cancer (CRC), and work in preclinical models has demonstrated a potential chemopreventive effect. Statins are also associated with reduced dysbiosis in the gut microbiome, yet the role of the gut microbiome in the protective effect of statins in CRC is unclear. Here we validated the chemopreventive role of statins by retrospectively analysing a cohort of patients who underwent colonoscopies. This was confirmed in preclinical models and patient cohorts, and we found that reduced tumour burden was partly due to statin modulation of the gut microbiota. Specifically, the gut commensal Lactobacillus reuteri was increased as a result of increased microbial tryptophan availability in the gut after atorvastatin treatment. Our in vivo studies further revealed that L. reuteri administration suppressed colorectal tumorigenesis via the tryptophan catabolite, indole-3-lactic acid (ILA). ILA exerted anti-tumorigenic effects by downregulating the IL-17 signalling pathway. This microbial metabolite inhibited T helper 17 cell differentiation by targeting the nuclear receptor, RAR-related orphan receptor γt (RORγt). Together, our study provides insights into an anti-cancer mechanism driven by statin use and suggests that interventions with L. reuteri or ILA could complement chemoprevention strategies for CRC.
2023-02-17 | GSE201452 | GEO
Project description:Epidemiological studies have indicated an association between statin use and reduced incidence of colorectal cancer (CRC), and work in preclinical models has demonstrated a potential chemopreventive effect. Statins are also associated with reduced dysbiosis in the gut microbiome, yet the role of the gut microbiome in the protective effect of statins in CRC is unclear. Here we validated the chemopreventive role of statins by retrospectively analysing a cohort of patients who underwent colonoscopies. This was confirmed in preclinical models and patient cohorts, and we found that reduced tumour burden was partly due to statin modulation of the gut microbiota. Specifically, the gut commensal Lactobacillus reuteri was increased as a result of increased microbial tryptophan availability in the gut after atorvastatin treatment. Our in vivo studies further revealed that L. reuteri administration suppressed colorectal tumorigenesis via the tryptophan catabolite, indole-3-lactic acid (ILA). ILA exerted anti-tumorigenic effects by downregulating the IL-17 signalling pathway. This microbial metabolite inhibited T helper 17 cell differentiation by targeting the nuclear receptor, RAR-related orphan receptor γt (RORγt). Together, our study provides insights into an anti-cancer mechanism driven by statin use and suggests that interventions with L. reuteri or ILA could complement chemoprevention strategies for CRC.
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Project description:Epidemiological studies have indicated an association between statin use and reduced incidence of colorectal cancer (CRC), and work in preclinical models has demonstrated a potential chemopreventive effect. Statins are also associated with reduced dysbiosis in the gut microbiome, yet the role of the gut microbiome in the protective effect of statins in CRC is unclear. Here we validated the chemopreventive role of statins by retrospectively analysing a cohort of patients who underwent colonoscopies. This was confirmed in preclinical models and patient cohorts, and we found that reduced tumour burden was partly due to statin modulation of the gut microbiota. Specifically, the gut commensal Lactobacillus reuteri was increased as a result of increased microbial tryptophan availability in the gut after atorvastatin treatment. Our in vivo studies further revealed that L. reuteri administration suppressed colorectal tumorigenesis via the tryptophan catabolite, indole-3-lactic acid (ILA). ILA exerted anti-tumorigenic effects by downregulating the IL-17 signalling pathway. This microbial metabolite inhibited T helper 17 cell differentiation by targeting the nuclear receptor, RAR-related orphan receptor γt (RORγt). Together, our study provides insights into an anti-cancer mechanism driven by statin use and suggests that interventions with L. reuteri or ILA could complement chemoprevention strategies for CRC.
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Project description:This SuperSeries is composed of the following subset Series: GSE11860: The impact of glycerol on the metabolism of Lactobacillus reuteri - Exploratory experiment GSE11861: The impact of glycerol on the metabolism of Lactobacillus reuteri - Main experiment Refer to individual Series
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Project description:Lactobacillus reuteri 100-23 is an autochthonous inhabitant of the rodent gastrointestinal system that adheres to the non-secretory epithelium of the forestomach and forms biofilms. Microarray analysis of the expression profile of L. reuteri 100-23 cells harvested from the stomach of ex-Lactobacillus-free mice, compared to those of L. reuteri 100-23 in laboratory culture, revealed an in vivo upregulation of a urease gene cluster by greater than 50-fold. Genes for urease production were absent in all publically available Lactobacillus genome sequences except L. reuteri 100-23 and have recently been identified as specific to rodent strains of L. reuteri (Frese et al. 2011). In the current study, the urease enzyme was shown to be functional. Supplementation with 2% urea allowed L. reuteri 100-23 to increase the pH of the culture medium. A mutant strain of L. reuteri 100-23 was developed by insertional inactivation of the ureC gene, which encodes the largest subunit of the urease enzyme. The mutant strain was unable to hydrolyze urea to increase the pH of culture medium, and did not survive acid stress at pH 2.5 for 6 h, even in the presence of urea. In contrast, the wild type strain was still viable after 6 h when 2% urea supplementation was included. When mice free of lactobacilli were inoculated with a mixture of equal numbers of wild type L. reuteri 100-23 and ureC mutant cells, the wild type constituted 99% of the resulting Lactobacillus population in the stomach, caecum and jejunum after one week (108 cells/gram of sample). This study has therefore shown the importance of a functional urease enzyme in the ecological fitness of L. reuteri 100-23.
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Project description:We performed 10x single cell RNA-seq on sorted populations: T cell (7AAD- Calcein blue+ CD45+ THY1.1- TCRb+), fibroblasts (7AAD- Calcein Blue+ CD45- THY1.1- CD31- PDPN+), myeloid cells (7AAD- Calcein Blue+ CD45+ THY1.1- CD11b+) and tumor cells (7AAD- Calcein Blue+ CD45- THY1.1+) from cells in an orthotopic EMT6 tumor model 7 days after treatment initiation in four experimental groups: 1) Control 2) aPD-L1 3) aTGFb 4) aPD-L1 and aTGFb.
2023-06-30 | E-MTAB-13072 | biostudies-arrayexpress
Project description:Lactobacillus reuteri 100-23 is an autochthonous inhabitant of the rodent gastrointestinal system that adheres to the non-secretory epithelium of the forestomach and forms biofilms. Microarray analysis of the expression profile of L. reuteri 100-23 cells harvested from the stomach of ex-Lactobacillus-free mice, compared to those of L. reuteri 100-23 in laboratory culture, revealed an in vivo upregulation of a urease gene cluster by greater than 50-fold. Genes for urease production were absent in all publically available Lactobacillus genome sequences except L. reuteri 100-23 and have recently been identified as specific to rodent strains of L. reuteri (Frese et al. 2011). In the current study, the urease enzyme was shown to be functional. Supplementation with 2% urea allowed L. reuteri 100-23 to increase the pH of the culture medium. A mutant strain of L. reuteri 100-23 was developed by insertional inactivation of the ureC gene, which encodes the largest subunit of the urease enzyme. The mutant strain was unable to hydrolyze urea to increase the pH of culture medium, and did not survive acid stress at pH 2.5 for 6 h, even in the presence of urea. In contrast, the wild type strain was still viable after 6 h when 2% urea supplementation was included. When mice free of lactobacilli were inoculated with a mixture of equal numbers of wild type L. reuteri 100-23 and ureC mutant cells, the wild type constituted 99% of the resulting Lactobacillus population in the stomach, caecum and jejunum after one week (108 cells/gram of sample). This study has therefore shown the importance of a functional urease enzyme in the ecological fitness of L. reuteri 100-23. Analysis of the microarray data was obtained from two independent biological replicates.
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