Mice intestinal microbiome
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ABSTRACT:
PROVIDER: PRJEB29020 | ENA |
REPOSITORIES: ENA
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Project description:Metagenomic and Metatranscriptomic analysis of mice intestinal microbiome
| PRJEB33889 | ENA
Project description:Objectives: Obstructive Sleep Apnea (OSA) is related to repeated upper airway collapse, intermittent hypoxia, and intestinal barrier dysfunction. The resulting damage to the intestinal barrier may affect or be affected by the intestinal microbiota. Methods: A prospective case-control was used, including 48 subjects from Sleep Medicine Center of Nanfang Hospital. Sleep apnea was diagnosed by overnight polysomnography. Fecal samples and blood samples were collected from subjects to detect intestinal microbiome composition (by 16S rDNA gene amplification and sequencing) and intestinal barrier biomarkers – intestinal fatty acid-binding protein (I-FABP) and D-lactic acid (D-LA) (by ELISA and colorimetry, respectively). Results: The severity of OSA was related to differences in the structure and composition of the intestinal microbiome. Enriched Fusobacterium, Megamonasa, Lachnospiraceae_UCG_006, and reduced Anaerostipes was found in patients with severe OSA. Enriched Ruminococcus_2, Lachnoclostridium, Lachnospiraceae_UCG_006, and Alloprevotella was found in patients with high intestinal barrier biomarkers. Lachnoclostridium and Lachnospiraceae_UCG_006 were the common dominant bacteria of OSA and intestinal barrier damage. Fusobacterium and Peptoclostridium was independently associated with apnea-hypopnea index (AHI). The dominant genera of severe OSA were also related to glucose, lipid, neutrophils, monocytes and BMI. Network analysis identified links between the intestinal microbiome, intestinal barrier biomarkers, and AHI. Conclusions: The study confirms that changes in the intestinal microbiota are related to intestinal barrier biomarkers among patients in OSA. These changes may play a pathophysiological role in the systemic inflammation and metabolic comorbidities associated with OSA, leading to multi-organ morbidity of OSA.
2023-08-30 | GSE181270 | GEO
Project description:IL-17 and IL-17R signaling in the intestinal epithelium regulate the intestinal microbiome. Given the reported links between intestinal dysbiosis, bacterial translocation, and liver disease, we hypothesized that intestinal IL-17R signaling plays a critical role in mitigating hepatic inflammation. To test this, we studied intestinal epithelial-specific IL-17RA deficient mice in a model of concanavalin A hepatitis. Absence of enteric IL-17RA signaling exacerbated hepatitis and hepatocyte cell death. These mice exhibited commensal dysbiosis, increased intestinal and liver Il18, and increased liver translocation of bacterial products, specifically CpG DNA. Mechanistically, CpG DNA induced hepatic IL-18, increasing IFNγ and FasL in hepatic T-cells to drive inflammation. Thus, intestinal IL-17R regulates translocation of TLR9 ligands and constrains susceptibility to hepatitis. These data connect enteric Th17 signaling and the microbiome in hepatitis, with broader implications on the effects of impaired intestinal immunity and subsequent release of microbial products seen in other extra-intestinal pathologies.
2019-12-10 | GSE128284 | GEO
Project description:The intestinal microbiome was examined from fecal pellets of animals with genetic targeting of the BTLA inhibitory receptor and the TNFR superfamily member HVEM, or in animals treated with agonist antibodies specific for BTLA.
2022-02-08 | GSE195890 | GEO
Project description:With annually 2.56 million deaths worldwide, pneumonia is one of the leading causes of death. Most frequent causative pathogens are Streptococcus pneumoniae and influenza A virus. Lately, the interaction between pathogens, the host and its microbiome gained more attention. A healthy microbiome is known to enhance the immune response towards pathogens, however, our knowledge on how infections affect the microbiome is still scarce. In this study, a meta-omics approach was used to investigate the impact of S. pneumoniae and influenza A virus infection on structure and function of the respiratory and gastrointestinal microbiomes of mice. In particular, the taxonomic composition of the respiratory microbiome was less affected by bacterial colonization and viral infection compared to S. pneumoniae infection. Pneumococcal pneumonia led to reduction of bacterial families and lower diversity in the respiratory microbiome, whereas diversity/richness was unaffected following H1N1 infection. Within the gastrointestinal microbiome we found exclusive changes in structure and function depending on the pneumonia inducing pathogen. Exemplarily, increased abundance of Akkermansiaceae and Spirochaetaceae, as well as decreased amounts of Clostridiaceae in response to S. pneumoniae infection, while increased presence of Enterococcaceae and Staphylococcaceae was specific for viral-induced pneumonia. Investigation of the intestinal microbiomes functional composition revealed reduced expression of flagellin and rubrerythrin and increased levels of ATPase during pneumococcal infection, while increased amounts of acetyl-CoA acetyltransferase and, enoyl-CoA transferase were unique after H1N1 infection. The identification of specific taxonomical and functional profiles during infection with a respective pathogen could deliver new insights in the role of the microbiome during disease and be beneficial for discrimination of pneumococcal- or viral-induced pneumonia.
2023-03-24 | PXD036129 | Pride
Project description:With annually 2.56 million deaths worldwide, pneumonia is one of the leading causes of death. Most frequent causative pathogens are Streptococcus pneumoniae and influenza A virus. Lately, the interaction between pathogens, the host and its microbiome gained more attention. A healthy microbiome is known to enhance the immune response towards pathogens, however, our knowledge on how infections affect the microbiome is still scarce. In this study, a meta-omics approach was used to investigate the impact of S. pneumoniae and influenza A virus infection on structure and function of the respiratory and gastrointestinal microbiomes of mice. In particular, the taxonomic composition of the respiratory microbiome was less affected by bacterial colonization and viral infection compared to S. pneumoniae infection. Pneumococcal pneumonia led to reduction of bacterial families and lower diversity in the respiratory microbiome, whereas diversity/richness was unaffected following H1N1 infection. Within the gastrointestinal microbiome we found exclusive changes in structure and function depending on the pneumonia inducing pathogen. Exemplarily, increased abundance of Akkermansiaceae and Spirochaetaceae, as well as decreased amounts of Clostridiaceae in response to S. pneumoniae infection, while increased presence of Enterococcaceae and Staphylococcaceae was specific for viral-induced pneumonia. Investigation of the intestinal microbiomes functional composition revealed reduced expression of flagellin and rubrerythrin and increased levels of ATPase during pneumococcal infection, while increased amounts of acetyl-CoA acetyltransferase and, enoyl-CoA transferase were unique after H1N1 infection. The identification of specific taxonomical and functional profiles during infection with a respective pathogen could deliver new insights in the role of the microbiome during disease and be beneficial for discrimination of pneumococcal- or viral-induced pneumonia.
2023-03-24 | PXD036279 | Pride
Project description:With annually 2.56 million deaths worldwide, pneumonia is one of the leading causes of death. Most frequent causative pathogens are Streptococcus pneumoniae and influenza A virus. Lately, the interaction between pathogens, the host and its microbiome gained more attention. A healthy microbiome is known to enhance the immune response towards pathogens, however, our knowledge on how infections affect the microbiome is still scarce. In this study, a meta-omics approach was used to investigate the impact of S. pneumoniae and influenza A virus infection on structure and function of the respiratory and gastrointestinal microbiomes of mice. In particular, the taxonomic composition of the respiratory microbiome was less affected by bacterial colonization and viral infection compared to S. pneumoniae infection. Pneumococcal pneumonia led to reduction of bacterial families and lower diversity in the respiratory microbiome, whereas diversity/richness was unaffected following H1N1 infection. Within the gastrointestinal microbiome we found exclusive changes in structure and function depending on the pneumonia inducing pathogen. Exemplarily, increased abundance of Akkermansiaceae and Spirochaetaceae, as well as decreased amounts of Clostridiaceae in response to S. pneumoniae infection, while increased presence of Enterococcaceae and Staphylococcaceae was specific for viral-induced pneumonia. Investigation of the intestinal microbiomes functional composition revealed reduced expression of flagellin and rubrerythrin and increased levels of ATPase during pneumococcal infection, while increased amounts of acetyl-CoA acetyltransferase and, enoyl-CoA transferase were unique after H1N1 infection. The identification of specific taxonomical and functional profiles during infection with a respective pathogen could deliver new insights in the role of the microbiome during disease and be beneficial for discrimination of pneumococcal- or viral-induced pneumonia.
2023-03-24 | PXD036115 | Pride
Project description:With annually 2.56 million deaths worldwide, pneumonia is one of the leading causes of death. Most frequent causative pathogens are Streptococcus pneumoniae and influenza A virus. Lately, the interaction between pathogens, the host and its microbiome gained more attention. A healthy microbiome is known to enhance the immune response towards pathogens, however, our knowledge on how infections affect the microbiome is still scarce. In this study, a meta-omics approach was used to investigate the impact of S. pneumoniae and influenza A virus infection on structure and function of the respiratory and gastrointestinal microbiomes of mice. In particular, the taxonomic composition of the respiratory microbiome was less affected by bacterial colonization and viral infection compared to S. pneumoniae infection. Pneumococcal pneumonia led to reduction of bacterial families and lower diversity in the respiratory microbiome, whereas diversity/richness was unaffected following H1N1 infection. Within the gastrointestinal microbiome we found exclusive changes in structure and function depending on the pneumonia inducing pathogen. Exemplarily, increased abundance of Akkermansiaceae and Spirochaetaceae, as well as decreased amounts of Clostridiaceae in response to S. pneumoniae infection, while increased presence of Enterococcaceae and Staphylococcaceae was specific for viral-induced pneumonia. Investigation of the intestinal microbiomes functional composition revealed reduced expression of flagellin and rubrerythrin and increased levels of ATPase during pneumococcal infection, while increased amounts of acetyl-CoA acetyltransferase and, enoyl-CoA transferase were unique after H1N1 infection. The identification of specific taxonomical and functional profiles during infection with a respective pathogen could deliver new insights in the role of the microbiome during disease and be beneficial for discrimination of pneumococcal- or viral-induced pneumonia.
2023-03-24 | PXD036014 | Pride
Project description:The gastric barrier plays a major role in the maintanance of the distal intestinal microbiome composition. It has been shown before that the use of gastric acid suppression medication, such as proton pump inhibitors, are associated with distinctive alterations of the intestinal microbiome. Foremost, the invasion of predominantly oral bacteria, like Veillonella and Streptococcus species, were a resurring finding in previous reports.
Gastric cancer treatment includes the total or subtotal resection of the stomach which can influence the gastric acid production. However, the influence by alterations in gastric milieu after this treatment on the composition of the intestinal microbiome is not well studied.
Therefore, the intestinal microbiome of patients after total or subtotal gastrectomy and its influence on intestinal inflammation and gut permeability will be studied.
| 2264742 | ecrin-mdr-crc
Project description:A human gut-on-a-chip microdevice was used to coculture multiple commensal microbes in contact with living human intestinal epithelial cells for more than a week in vitro and to analyze how gut microbiome, inflammatory cells, and peristalsis-associated mechanical deformations independently contribute to intestinal bacterial overgrowth and inflammation. This in vitro model replicated results from past animal and human studies, including demonstration that probiotic and antibiotic therapies can suppress villus injury induced by pathogenic bacteria. By ceasing peristalsis-like motions while maintaining luminal flow, lack of epithelial deformation was shown to trigger bacterial overgrowth similar to that observed in patients with ileus and inflammatory bowel disease. Analysis of intestinal inflammation on-chip revealed that immune cells and lipopolysaccharide endotoxin together stimulate epithelial cells to produce four proinflammatory cytokines (IL-8, IL-6, IL-1β, and TNF-α) that are necessary and sufficient to induce villus injury and compromise intestinal barrier function. Thus, this human gut-on-a-chip can be used to analyze contributions of microbiome to intestinal pathophysiology and dissect disease mechanisms in a controlled manner that is not possible using existing in vitro systems or animal models. 6 samples, 2 biological replicates for each 3 conditions.
2015-12-16 | E-GEOD-65790 | biostudies-arrayexpress