Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1282887 | ENA |
REPOSITORIES: ENA
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Project description:Pulmonary fibrosis is a chronic progressive and often fatal disease. The pathogenesis is characterized by aberrant repair and remodeling of the lung parenchyma resulting in loss of physiological homeostasis, respiratory failure and death. The immune response in pulmonary fibrosis is dysregulated. The gut microbiome is a key regulator of immunity. The role of the gut microbiome in regulating the pulmonary immunity in lung fibrosis is unknown. Here, we have utilized a strategy of cage randomization to study how the horizontal transmission of gut microbiome influences the development of pulmonary fibrosis.
2022-07-29 | GSE209784 | GEO
Project description:Azithromycin (AZM) reduces pulmonary inflammation and exacerbations in chronic obstructive pulmonary disease patients with emphysema. The antimicrobial effects of AZM on the lung microbiome are not known and may contribute to its beneficial effects. Methods. Twenty smokers with emphysema were randomized to receive AZM 250 mg or placebo daily for 8 weeks. Bronchoalveolar lavage (BAL) was performed at baseline and after treatment. Measurements included: rDNA gene quantity and sequence. Results. Compared with placebo, AZM did not alter bacterial burden but reduced α-diversity, decreasing 11 low abundance taxa, none of which are classical pulmonary pathogens. Conclusions. AZM treatment the lung microbiome Randomized trial comparing azithromycin (AZM) treatment with placebo for eight weeks. Bronchoalveolar lavage (BAL) samples were obtained before and after treatment to explore the effects of AZM on microbiome, in the lower airways. 16S rRNA was quantified and sequenced (MiSeq) The amplicons from total 39 samples are barcoded and the barcode is provided in the metadata_complete.txt file.
2016-07-19 | E-GEOD-74396 | biostudies-arrayexpress
Project description:Pulmonary enteric adenocarcinoma (PEAD) is a rare non-small cell lung cancer subtype. It is poorly characterized and cannot be distinguished from metastatic colorectal or upper gastrointestinal adenocarcinomas (ADCs) by means of routine pathological methods. As DNA methylation patterns are known to be highly tissue specific, we aimed to develop a methylation-based algorithm to differentiate these entities. To this end, genome wide methylation profiles of 600 primary pulmonary, colorectal and upper gastrointestinal ADCs obtained from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) database were used as a reference cohort to train a machine learning algorithm. The resulting classifier correctly classified all samples from a validation cohort consisting of 680 primary pulmonary, colorectal and upper gastrointestinal ADCs from TCGA and the GEO database, demonstrating the ability of the algorithm to reliably distinguish these three entities. We then analyzed DNA methylation data of 15 PEADs as well as four pulmonary metastases and four primary colorectal ADCs with the algorithm. All 15 PEADs were reliably classified as primary pulmonary tumors and all four metastases as well as all four primary colorectal ADC samples were identified as primary colorectal ADCs. In a t-distributed stochastic neighbor embedding analysis, the PEAD samples did not form a separate methylation subclass but rather diffusely intermixed with other pulmonary ADCs. Additional characterization of the PEAD series using fluorescence in-situ hybridization, next generation sequencing and copy number analysis revealed KRAS mutations in nine of 15 samples (60%) and a high number of structural chromosomal changes. Except for an unusually high rate of chromosome 20 gain (66.7%) the molecular data was mostly reminiscent of standard pulmonary ADCs. In conclusion, we provide sound evidence of the pulmonary origin of PEAD and in addition provide a publicly available machine learning based algorithm to reliably distinguish PEAD from metastatic colorectal cancer and upper gastrointestinal adenocarcinomas.
2019-01-04 | GSE116699 | GEO
Project description:The gut microbiome has been implicated in multiple human chronic gastrointestinal (GI) disorders. Determining its mechanistic role in disease pathogenesis has been difficult due to the apparent disconnect between animal and human studies and a lack of an integrated multi-omics view in the context of disease-specific physiological changes. We integrated longitudinal multi-omics data from the gut microbiome, metabolome, host epigenome and transcriptome in the context of irritable bowel syndrome (IBS) host physiology. We identified IBS subtype-specific and symptom-related variation in microbial composition and function. A subset of identified changes in microbial metabolites correspond to host physiological mechanisms that are relevant to IBS. By integrating multiple data layers, we identified purine metabolism as a novel host-microbial metabolic pathway in IBS with translational potential. Our study highlights the importance of longitudinal sampling and integrating complementary multi-omics data to identify functional mechanisms that can serve as therapeutic targets in a comprehensive treatment strategy for chronic GI diseases.
2020-03-13 | GSE146853 | GEO
Project description:During cancer evolution, cellular differentiation programs become dysregulated. The transcription factor Nkx2-1 is a master regulator of pulmonary differentiation that is downregulated in poorly differentiated lung adenocarcinoma. Here we use conditional murine genetics to study the fate of lung epithelial cells upon loss of their master cell fate regulator. Nkx2-1 deletion in normal and neoplastic lung causes not only loss of pulmonary identity but also gastric transdifferentiation. Nkx2-1 maintains pulmonary identity by sequestering the Foxa1 transcription factor at lung-specific loci and inhibiting Foxa1 binding to gastrointestinal targets. Murine Nkx2-1-negative lung tumors mimic the mucinous subtype of human lung adenocarcinoma, which also exhibits gastric transdifferentiation. Nkx2-1-negative lung adenocarcinomas are dependent on the gastrointestinal gene Hnf4a for efficient initiation. Thus, loss of Nkx2-1 results in transdifferentiation rather than stable dedifferentiation in vivo, suggesting that inactivation of both active and latent differentiation programs may be required for tumors to reach a primitive, dedifferentiated state. The study was designed to compare the expression profiles of Nkx2-1-positive lung adenocarcinomas with tumors in which Nkx2-1 was deleted at the time of initiation or 6-7 months after initiation.
2013-04-10 | E-GEOD-36473 | biostudies-arrayexpress
Project description:Azithromycin (AZM) reduces pulmonary inflammation and exacerbations in chronic obstructive pulmonary disease patients with emphysema. The antimicrobial effects of AZM on the lung microbiome are not known and may contribute to its beneficial effects. Methods. Twenty smokers with emphysema were randomized to receive AZM 250 mg or placebo daily for 8 weeks. Bronchoalveolar lavage (BAL) was performed at baseline and after treatment. Measurements included: rDNA gene quantity and sequence. Results. Compared with placebo, AZM did not alter bacterial burden but reduced α-diversity, decreasing 11 low abundance taxa, none of which are classical pulmonary pathogens. Conclusions. AZM treatment the lung microbiome
2016-07-19 | GSE74396 | GEO
Project description:During cancer evolution, cellular differentiation programs become dysregulated. The transcription factor Nkx2-1 is a master regulator of pulmonary differentiation that is downregulated in poorly differentiated lung adenocarcinoma. Here we use conditional murine genetics to study the fate of lung epithelial cells upon loss of their master cell fate regulator. Nkx2-1 deletion in normal and neoplastic lung causes not only loss of pulmonary identity but also gastric transdifferentiation. Nkx2-1 maintains pulmonary identity by sequestering the Foxa1 transcription factor at lung-specific loci and inhibiting Foxa1 binding to gastrointestinal targets. Murine Nkx2-1-negative lung tumors mimic the mucinous subtype of human lung adenocarcinoma, which also exhibits gastric transdifferentiation. Nkx2-1-negative lung adenocarcinomas are dependent on the gastrointestinal gene Hnf4a for efficient initiation. Thus, loss of Nkx2-1 results in transdifferentiation rather than stable dedifferentiation in vivo, suggesting that inactivation of both active and latent differentiation programs may be required for tumors to reach a primitive, dedifferentiated state.
2013-04-10 | GSE36473 | GEO
Project description:Tissue-specific differentiation programs become dysregulated during cancer evolution. The transcription factor Nkx2-1 is a master regulator of pulmonary differentiation that is downregulated in poorly differentiated lung adenocarcinoma. Here we use conditional murine genetics to study the fate of lung epithelial cells upon loss of their master cell fate regulator. Nkx2-1 deletion in normal and neoplastic lung causes not only loss of pulmonary identity but also gastric transdifferentiation. Nkx2-1 maintains pulmonary identity by sequestering the Foxa1 transcription factor at lung-specific loci and by inhibiting Foxa1 binding to gastrointestinal targets. Murine Nkx2-1-negative lung tumors mimic the mucinous subtype of human lung adenocarcinoma, which also exhibits gastric transdifferentiation. Nkx2-1-negative lung adenocarcinomas are dependent on the gastrointestinal gene Hnf4a for efficient initiation. Thus, loss of Nkx2-1 causes transdifferentiation rather than stable dedifferentiation in vivo, suggesting that inactivation of both active and latent differentiation programs are required for tumors to reach a primitive, dedifferentiated state.
2013-04-09 | GSE43252 | GEO
Project description:Seasonal influenza outbreaks represent a large burden for the healthcare system as well as the economy. While the role of the microbiome in the context of various diseases has been elucidated, the effects on the respiratory and gastrointestinal microbiome during influenza illness is largely unknown. Therefore, this study aimed to characterize the temporal development of the respiratory and gastrointestinal microbiome of swine using a multi-omics approach prior and during influenza infection. Swine is a suitable animal model for influenza research, as it is closely related to humans and a natural host for influenza viruses. Our results showed that IAV infection resulted in significant changes in the abundance of Moraxellaceae and Pasteurellaceae families in the upper respiratory tract. To our surprise, temporal development of the respiratory microbiome was not affected. Furthermore, we observed significantly altered microbial richness and diversity in the gastrointestinal microbiome after IAV infection. In particular, we found increased abundances of Prevotellaceae, while Clostridiaceae and Lachnospiraceae decreased. Furthermore, metaproteomics showed that the functional composition of the microbiome, known to be robust and stable under healthy conditions, was heavily affected by the influenza infection. Metabolome analysis proved increased amounts of short-chain fatty acids in the gastrointestinal tract, which might be involved in faster recovery. Furthermore, metaproteome data suggest a possible immune response towards flagellated Clostridia induced during the infection. Therefore, it can be assumed that the respiratory infection with IAV caused a systemic effect in the porcine host and microbiome.
2022-02-16 | PXD024077 | Pride