Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1079906 | ENA |
REPOSITORIES: ENA
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Project description:We found that low protein diet consumption resulted in decrease in the percentage of normal Paneth cell population in wild type mice, indicating that low protein diet could negatively affect Paneth cell function. We performed fecal microbiota composition profiling. Male mice were used at 4-5 weeks of age. Fecal samples were collected for microbiome analysis.
2023-07-02 | E-MTAB-11277 | biostudies-arrayexpress
Project description:Opioids such as morphine have many beneficial properties as analgesics, however, opioids may induce multiple adverse gastrointestinal symptoms. We have recently demonstrated that morphine treatment results in significant disruption in gut barrier function leading to increased translocation of gut commensal bacteria. However, it is unclear how opioids modulate the gut homeostasis. By using a mouse model of morphine treatment, we studied effects of morphine treatment on gut microbiome. We characterized phylogenetic profiles of gut microbes, and found a significant shift in the gut microbiome and increase of pathogenic bacteria following morphine treatment when compared to placebo. In the present study, wild type mice (C57BL/6J) were implanted with placebo, morphine pellets subcutaneously. Fecal matter were taken for bacterial 16s rDNA sequencing analysis at day 3 post treatment. A scatter plot based on an unweighted UniFrac distance matrics obtained from the sequences at OTU level with 97% similarity showed a distinct clustering of the community composition between the morphine and placebo treated groups. By using the chao1 index to evaluate alpha diversity (that is diversity within a group) and using unweighted UniFrac distance to evaluate beta diversity (that is diversity between groups, comparing microbial community based on compositional structures), we found that morphine treatment results in a significant decrease in alpha diversity and shift in fecal microbiome at day 3 post treatment compared to placebo treatment. Taxonomical analysis showed that morphine treatment results in a significant increase of potential pathogenic bacteria. Our study shed light on effects of morphine on the gut microbiome, and its role in the gut homeostasis.
2018-04-16 | E-MTAB-5546 | biostudies-arrayexpress
Project description:We found that western diet consumption resulted in decrease in the percentage of normal Paneth cell population in wild type mice, indicating that western diet could negatively affect Paneth cell function. Subsequent generations of western diet consumption further reduced percentages of normal Paneth cell population. We performed fecal microbiota composition profiling. Male mice were used at 4-5 weeks of age. Fecal samples were collected for microbiome analysis.
2023-01-01 | E-MTAB-10995 | biostudies-arrayexpress
Project description:Morphine causes microbial dysbiosis. In this study we focused on restoration of native microbiota in morphine treated mice and looked at the extent of restoration and immunological consequences of this restoration. Fecal transplant has been successfully used clinically, especially for treating C. difficile infection2528. With our expanding knowledge of the central role of microbiome in maintenance of host immune homeostasis17, fecal transplant is gaining importance as a therapy for indications resulting from microbial dysbiosis. There is a major difference between fecal transplant being used for the treatment of C. difficile infection and the conditions described in our studies. The former strategy is based on the argument that microbial dysbiosis caused by disproportionate overgrowth of a pathobiont can be out-competed by re-introducing the missing flora by way of a normal microbiome transplant. This strategy is independent of host factors and systemic effects on the microbial composition. Here, we show that microbial dysbiosis caused due to morphine can be reversed by transplantation of microbiota from the placebo-treated animals.
2016-06-01 | E-MTAB-3723 | biostudies-arrayexpress
Project description:Microbiota dysbiosis and mucosa-associated bacteria are involved in colorectal cancer progression. We hypothesized that a time-specific interaction between dysbiotic pathobionts and host responses promote tumor growth. This study aimed to elucidate the dysfunctional host-microbe interplay in colon tumorigenesis by using a time-series metagenomics approach. A transient surge in fecal microbial richness was linked to a unique transcriptome profile in the mouse colon during carcinoma transformation. Monitoring gut microbiome may help identifying the window-of-opportunity to induce tumor regression using bacteria-targeted precision medicine.
2021-11-24 | GSE166038 | GEO
Project description:Microbiota dysbiosis and mucosa-associated bacteria are involved in colorectal cancer progression. We hypothesized that a time-specific interaction between dysbiotic pathobionts and host responses promote tumor growth. This study aimed to elucidate the dysfunctional host-microbe interplay in colon tumorigenesis by using a time-series metagenomics approach. A transient surge in fecal microbial richness was linked to a unique transcriptome profile in the mouse colon during carcinoma transformation. Monitoring gut microbiome may help identifying the window-of-opportunity to induce tumor regression using bacteria-targeted precision medicine.
2021-11-24 | GSE166030 | GEO
Project description:DNA methylation is an epigenetic mark that is altered in cancer and aging tissues. The effects of extrinsic factors on DNA methylation remain incompletely understood. Microbial dysbiosis is a hallmark of colorectal cancer, and infections have been linked to aberrant DNA methylation in cancers of the GI tract. To determine the microbiota’s impact on DNA methylation, we studied the DNA methylation of colorectal mucosa in germ-free (GF, no microbiome) and specific pathogen free (SPF, controlled microbiome) mice, as well as in interleukin 10 KO mice (Il10-/-) which are prone to inflammation and tumorigenesis in the presence of a microbiome. We compared DNA methylation changes to those seen in aging, and after exposure to the colon carcinogen azoxymethane (AOM). DNA methylation changes associated with aging were accelerated in the Il10-/- /SPF mice. By contrast, AOM induced profound hypomethylation that was distinct from the effects of aging or of the microbiome. CpG sites modified by the microbiome were over-represented among DNA methylation changes in colorectal cancer. Thus, the microbiome affects the DNA methylome of colorectal mucosa in patterns reminiscent of what is observed in colorectal cancer.
2023-05-09 | GSE150333 | GEO
Project description:analysis of fecal samples in colorectal cancer Egyptians patients
2023-08-18 | PXD037271 | Pride
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.
2020-11-30 | E-MTAB-8739 | biostudies-arrayexpress
Project description:We examined fecal proteins from normal subjects (n=6), patients with inflammatory bowel disease (n=8), patients with colorectal adenoma (n=8), and patients with colorectal cancer (n=14) in the hope of identifying novel fecal protein markers that could be used to identify colorectal diseases.
2022-12-22 | PXD039089 |