Ontology highlight
ABSTRACT:
PROVIDER: PRJNA680896 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13149600.fastq.gz | Fastqsanger.gz | |||
| SRR13149601.fastq.gz | Fastqsanger.gz | |||
| SRR13149602.fastq.gz | Fastqsanger.gz | |||
| SRR13149603.fastq.gz | Fastqsanger.gz | |||
| SRR13149604.fastq.gz | Fastqsanger.gz |
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Project description:Proteome analysis of Lung tissue of mice bearing B16-F10-luc-G5 melanoma tumor with sleep fragmentation and with or with out the asdmistration of GL-pp. The mice were randomly divided into 4 groups: control group in general condition with no further treatment (CON group), tumor group with the burden of B16-F10-luc-G5 cells (Tumor group), T+SF group with SF and the burden of B16-F10-luc-G5 cells (T+SF group), and GL-pp group with SF, tumor cells burden, and the administration of 80 mg/kg GL-pp (GL-pp group). B16-F10-luc-G5 cells (5 × 1000000 cells/100 µL per mouse) were injected into the mice through the tail vein. The lung tissue of T+SF group and GL-pp group were analyzed by the proteome.
2021-09-10 | PXD025171 | Pride
Project description:Introduction: Chronic sleep fragmentation (SF) is prevalent in contemporary human society, highlighting detrimental effects on glucose metabolism and adipose tissue morphology, which is closely linked to gut microbiota composition. However, it remains unclear whether sleep recovery (SR) after prolonged SF can ameliorate glucose metabolism, influence the transcriptome of inguinal white adipose tissue (iWAT), and whether these effects align with alterations in the gut microbiota. Methods: Mice were subjected to 8 weeks of SF and subsequently allowed 2 weeks of SR. We assessed glucose tolerance through intraperitoneal glucose tolerance tests (ipGTT), analyzed gut microbiota via 16s rDNA amplicon sequencing, and examined transcriptomic alterations in iWAT using RNA sequencing. Results: Despite the two-week SR following chronic SF, significant glucose intolerance persisted, accompanied by subtle shifts in the gut microbiota and alterations in gene expression within iWAT. The top hub genes Ncapg, Cenpe, and Tik were identified from the protein-protein interaction network. Conclusion: Even followed by a brief period of SR, prolonged SF still led to ongoing glucose intolerance and alterations in the adipose tissue transcriptome in mice. These changes were intertwined with modifications in the gut microbiome. The shifts in gut microbiota may play a pivotal role in understanding the sustained negative effects of SF.
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Project description:Primary B cell receptor (BCR)/antibody variable region exons are generated by V(D)J recombination with junctional diversification creating immensely diverse antigen contact-encoding CDR3s. While most antigen-driven germinal centers (GCs) are transient, gut microbiota-dependent intestinal Peyer’s patch (PP) GCs are chronic. The nature of chronic PP GC BCR repertoires and somatic hyper-mutation (SHM) patterns has remained enigmatic. To elucidate the physiological repertoire of PP GC BCRs, we developed a high throughput antibody repertoire and SHM assay. Remarkably, PP GCs from different mice expanded public clonotypes, each often with identical IgH CDR3. These CDR3s represent innate-like BCRs that appear much more frequently than expected in naïve B cell repertoire by IGoR modeling, but not frequently enough to enter PP GCs at the observed recurrence without cellular selection. Consistently, some public clonotypes are gut microbiota-dependent and encode antibodies reactive to bacteria glycans, while others are not. SPF fecal transfer to germ-free (GF) mice restored two germ-dependent clonotypes, providing direct evidence for BCR selection. In support of this, we identified recurrently selected SHMs in four of the public clonotypes, demonstrating affinity maturation in chronic PP GCs. Our findings suggest that persistent gut antigens select for innate-like BCR clonotypes to seed chronic PP GCs.
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Project description:Recent studies in both mice and human have suggested that the gut microbiota could modulate tumor response to chemotherapeutic agents or immunotherapies. However, the underlying mechanism has not been well characterized. Here, we found that disruption of the intestinal microbiota with antibiotics impaired the anti-cancer efficacy of oxaliplatin, which was correlated with the reduction of lots of the intestinal microbial metabolites including butyrate, one of the short chain fatty acids. Re-supplementation of either the whole intestinal microbial metabolites or butyrate could rescue the therapeutic responses of oxaliplatin in the microbiota-destroyed tumor-bearing mice by modulating CD8+ T cell function in the tumor microenvironment. Further experiments showed butyrate boosted the anti-tumor cytotoxic CD8+ T cell responses through ID2, a key transcription regulator highly expressed by tumor-infiltrating CD8+ T cells. Butyrate induced ID2 expression in CD8+ T cells, while ID2 further promoted the proliferation and function of CD8+ T cells through IL-12 signaling. Together, our findings suggest that gut microbial metabolite butyrate could promote the anti-tumor therapeutic efficacy through the ID2-dependent regulation of CD8+ T cell immunity.
2021-03-24 | GSE115426 | GEO
Project description:Recent studies in both mice and human have suggested that the gut microbiota could modulate tumor response to chemotherapeutic agents or immunotherapies. However, the underlying mechanism has not been well characterized. Here, we found that disruption of the intestinal microbiota with antibiotics impaired the anti-cancer efficacy of oxaliplatin, which was correlated with the reduction of lots of the intestinal microbial metabolites including butyrate, one of the short chain fatty acids. Re-supplementation of either the whole intestinal microbial metabolites or butyrate could rescue the therapeutic responses of oxaliplatin in the microbiota-destroyed tumor-bearing mice by modulating CD8+ T cell function in the tumor microenvironment. Further experiments showed butyrate boosted the anti-tumor cytotoxic CD8+ T cell responses through ID2, a key transcription regulator highly expressed by tumor-infiltrating CD8+ T cells. Butyrate induced ID2 expression in CD8+ T cells, while ID2 further promoted the proliferation and function of CD8+ T cells through IL-12 signaling. Together, our findings suggest that gut microbial metabolite butyrate could promote the anti-tumor therapeutic efficacy through the ID2-dependent regulation of CD8+ T cell immunity.
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Project description:Background: Prevention of hyperlipidemia and associated diseases is a health priority. Complementary medicine based on scientific evidence has recently recognized the potential of natural products for modulating lipid metabolism, such as the medicinal mushroom Ganoderma lucidum (Gl), which possesses hypocholesterolemic, prebiotic and antidiabetic properties. Methods: Whole-transcriptomic changes in liver and kidney from a mouse model (C57BL/6), under a high-cholesterol diet and standardized Gl extracts (Gl-1, Gl-2) or simvastatin administration, were analyzed to determine Gl hypocholesterolemic activity. Further effects of Gl extracts on lipid metabolism were evaluated using an in vitro hepatic-like macrophage model. Additionally, correlations among hepatic gene expression, microbiota and serum lipid profiles in vivo established by Gl extracts were evaluated. Results: Based on the hepatic and renal mRNA profiles of mice treated with Gl extracts and high-cholesterol diet, we identified relevant metabolic pathways modulated by Gl involving the restriction of lipid biosynthesis and the enrichment of lipid degradation and secretion. We further showed that Gl extracts induce a significant decrease of macrophage lipid storage and cholesterol biosynthesis, which occurs concomitantly by the down-modulation of Fasn and Elovl6. We also determined that prebiotic effects of Gl extracts modulating gut microbiota are correlated with the gene expression portraits. Conclusions: Our high-throughput analysis allowed to identify key transcriptomic nodes established by Gl extracts and their interaction with microbiome composition related to lipid catabolic signaling. Our results indicated that our Gl extracts have a robust potential to be used as transcriptome modulators and prebiotic agents to prevent metabolic disorders associated to hypercholesterolemia.
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Project description:Pancreatic cancer is the 3rd most prevalent cause of cancer related deaths in United states alone, with over 55000 patients being diagnosed in 2019 alone and nearly as many succumbing to it. Late detection, lack of effective therapy and poor understanding of pancreatic cancer systemically contributes to its poor survival statistics. Obesity and high caloric intake linked co-morbidities like type 2 diabetes (T2D) have been attributed as being risk factors for a number of cancers including pancreatic cancer. Studies on gut microbiome has shown that lifestyle factors as well as diet has a huge effect on the microbial flora of the gut. Further, modulation of gut microbiome has been seen to contribute to effects of intensive insulin therapy in mice on high fat diet. In another study, abnormal gut microbiota was reported to contribute to development of diabetes in Db/Db mice. Recent studies indicate that microbiome and microbial dysbiosis plays a role in not only the onset of disease but also in its outcome. In colorectal cancer, Fusobacterium has been reported to promote therapy resistance. Certain intra-tumoral bacteria have also been shown to elicit chemo-resistance by metabolizing anti-cancerous agents. In pancreatic cancer, studies on altered gut microbiome have been relatively recent. Microbial dysbiosis has been observed to be associated with pancreatic tumor progression. Modulation of microbiome has been shown to affect response to anti-PD1 therapy in this disease as well. However, most of the studies in pancreatic cancer and microbiome have remained focused om immune modulation. In the current study, we observed that in a T2D mouse model, the microbiome changed significantly as the hyperglycemia developed in these animals. Our results further showed that, tumors implanted in the T2D mice responded poorly to Gemcitabine/Paclitaxel (Gem/Pac) standard of care compared to those in the control group. A metabolomic reconstruction of the WGS of the gut microbiota further revealed that an enrichment of bacterial population involved in drug metabolism in the T2D group.
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2015-02-12 | E-GEOD-51911 | biostudies-arrayexpress
Project description:The mammalian gut harbors a diverse microbial community (gut microbiota) that mainly consists of bacteria. Their combined genomes (the microbiome) provide biochemical and metabolic functions that complement host physiology. Maintaining symbiosis seems to be a key requirement for health as dysbiosis is associated with the development of common diseases. Previous studies indicated that the microbiota and the hostM-bM-^@M-^Ys epithelium signal bidirectional inducing transcriptional responses to fine-tune and maintain symbiosis. However, little is known about the hostM-bM-^@M-^Ys responses to the microbiota along the length of the gut as earlier studies of gut microbial ecology mostly used either colonic or fecal samples. This is of importance as not only function and architecture of the gut varies along its length but also microbial distribution and diversity. Few recent studies have begun to investigate microbiota-induced host responses along the length of the gut. However, these reports used whole tissue samples and therefore do not allow drawing conclusions about specificity of the observed responses. Which cells in the intestinal tissue are responsible for the microbially induced response: epithelial, mesenchymal or immune cells? Where are the responding cells located? We used using extensive microarray analysis of laser capture microdissection (LCM) harvested ileal and colonic tip and crypt fractions from germ-free and conventionally-raised mice to investigate the microbiota-induced transcriptional responses in specific and well-defined cell populations of the hostM-bM-^@M-^Ys epithelium. Ileum and colon segments were dissected from germ-free and conventionally-raised 10-12 weeks old female C57Bl/6 mice, washed and frozen as OCT blocks. Cryosections were prepared from these OCT blocks and tip/crypt fractions isolated using laser capture microdissection. To investigate the microbiota-induced transcriptional responses specific for specific subpopulations of intestinal epithelial cells, tip and crypt fractions of ileal and colonic epithelium of germ-free and conventionally-raised 10-12 weeks old female C57Bl/6 mice were harvested using laser capture microdissection and probed in an extensive microarray analysis.
2015-02-12 | E-GEOD-51910 | biostudies-arrayexpress