Respiratory airway microbiomes in stage I non-small cell lung cancer
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB34172 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3498980_1.fastq.gz | Fastqsanger.gz | |||
| ERR3498980_2.fastq.gz | Fastqsanger.gz | |||
| ERR3498990_1.fastq.gz | Fastqsanger.gz | |||
| ERR3498990_2.fastq.gz | Fastqsanger.gz | |||
| ERR3499000_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 142 |
Similar Datasets
Project description:Oral, respiratory airway, and lung tissue bacterial microbiomes in stage I non-small cell lung cancer
| PRJEB29934 | ENA
Project description:Microbiomes of bronchial lavage fluids of humans
| PRJEB41745 | ENA
Project description:The respiratory epithelium is a polarised layer at the interface between the outside environment and deeper lung structures, overlaid by the epithelial lining fluid (ELF). This provides a mechanical and immunological barrier to inhaled particulates, such as viruses. Human respiratory syncytial virus (hRSV) is a major cause of disease in humans, and targets the respiratory epithelium. However, little is known of the disruption of the ELF proteome in the context of virus-driven respiratory illnesses. To address this, a proteomics approach was combined with an ex-vivo human airway epithelial model (HAE) to investigate the apical and basolateral secretome in hRSV-infected cultures. This demonstrated that several apically- and basolaterally-restricted proteins were subsequently secreted in both directions upon infection, while a number of proteins saw their apical/basolateral abundance ratios significantly altered. Furthermore, another 35 proteins were uniquely identified after hRSV treatment. Importantly, some of these changes were correlated in nasal aspirates (NA) from children with and without hRSV. This study showed that hRSV could affect airway secretions, and disrupted the directionality of the respiratory epithelium.
2022-03-01 | PXD004430 | Pride
Project description:RNA was extracted from the meninges of mice from either Specific pathogen free or Germ free facilities or from the offspring of mice reconstituted with different human microbiomes.
2020-11-13 | GSE135620 | GEO
Project description:HuMiChip2 was applied to analyze perform both strain-level identification and the functional profiling of human gut microbiomes from alcoholic cirrhosis patients and healthy individuals with alcohol abuse.
2016-08-30 | GSE86162 | GEO
Project description:Chronic obstructive pulmonary disease (COPD) is a disease state characterized by poorly reversible, limited airflow that is usually both progressive and associated with an abnormal inflammatory response of the lung. One cause of COPD is chronic exposure to airborne materials such as cigarette smoke (CS), which leads to impaired respiratory function in damaged tissues. Damaged epithelial tissue initiates repair processes including proliferation and re-differentiation until there is complete regeneration of a pseudostratified epithelium. These repair processes in airway epithelial tissues are essential for maintaining normal airway function. However, impairment of epithelial repair leads to architectural changes through region-dependent remodeling processes that are associated with a fixed airflow limitation in COPD. To fully understand what factors mostly contribute to airway remodeling heterogeneity in COPD pathogenesis, we used two in vitro human airway epithelial 3D culture models, namely, MucilAir™ and SmallAir™ tissues, which are derived from large and small airway epithelial cells, respectively. To focus on regional heterogeneity of the respiratory tract, tissues from a single donor were used to eliminate potential donor-to-donor differences in responses to external stimuli. We exposed the tissues to different concentrations of whole CS (low, middle, and high), and examined the transcriptome at different post-exposure periods (4, 24, 48, and 72 h post-exposure).
2020-12-24 | E-MTAB-8680 | biostudies-arrayexpress
Project description:Airway integrity must be continuously maintained throughout life. Sensory neurons guard against airway obstruction and on a moment-by-moment basis, enact vital reflexes to maintain respiratory function. Decreased lung capacity is common and life-threatening across many respiratory diseases, and lung collapse can be acutely evoked by chest wall trauma, pneumothorax, or airway compression. Here, we characterize a neuronal reflex of the vagus nerve evoked by airway closure that leads to gasping. In vivo vagal ganglion imaging revealed dedicated sensory neurons that detect airway compression but not airway stretch. Vagal neurons expressing PVALB mediate airway closure responses, and innervate clusters of lung epithelial cells called neuroepithelial bodies (NEBs). Stimulating NEBs or vagal PVALB neurons evoked gasping in the absence of airway threats, while ablating NEBs or vagal PVALB neurons eliminated gasping to airway closure. Single-cell RNA sequencing revealed that NEBs uniformly express the mechanoreceptor PIEZO2, and targeted knockout of PIEZO2 in NEBs also eliminated responses to airway closure. NEBs are dispensable for the Hering-Breuer inspiratory reflex, indicating that discrete terminal structures detect airway closure and inflation. Like Merkel cells involved in touch sensation, NEBs are PIEZO2-expressing epithelial cells, and moreover, are critical for an aspect of lung mechanosensation. These findings expand our understanding of neuronal diversity in the airways, and reveal a dedicated vagal pathway that detects airway closure to help preserve respiratory function.
2024-03-06 | GSE252735 | GEO
Project description:We established a micro-patterned respiratory epithelial cell culture system in vitro. In this culture system, the iPSC-derived lung progenitor cells were differentiated into airway epithelial cells in a position-specific manner.
2024-02-29 | GSE236840 | GEO
Project description:The earliest morphologic evidence of changes in the airways associated with chronic cigarette smoking is in the small airways. To help understand how smoking modifies small airway structure and function, we developed a strategy using fiberoptic bronchoscopy and brushing to sample the human small airway (10th-12th order) bronchial epithelium to assess gene expression (Affymetrix HG-U133A array) in phenotypically normal smokers (n=6, 24 ± 4 pack-yr) compared to matched non-smokers (n=5). Compared to samples from the large (2nd to 3rd order) bronchi, the small airway samples had a higher proportion of ciliated cells, but less basal, undifferentiated, and secretory cells. The small, but not large, airway samples included Clara cells, a cell found only in the small airway epithelium, and the small, but not the large, airway epithelium expressed genes for the surfactant apoproteins. Despite the fact that the smokers were phenotypically normal, analysis of the small airway epithelium of the smokers compared to the non-smokers demonstrated up- and -down-regulation of genes in multiple categories relevant to the pathogenesis of chronic obstructive lung disease (COPD), including genes coding for cytokines/innate immunity, apoptosis, pro-fibrosis, mucin, responses to oxidants and xenobiotics, antiproteases and general cellular processes. In the context that COPD starts in the small airways, these changes in gene expression in the small airway epithelium in phenotypically normal smokers are candidates for the development of therapeutic strategies to prevent the onset of COPD. Keywords: response to cigarette smoking
2005-10-30 | GSE3320 | GEO
Project description:Modification of Gene Expression of the Small Airway Epithelium in Response to Cigarette Smoking The earliest morphologic evidence of changes in the airways associated with chronic cigarette smoking is in the small airways. To help understand how smoking modifies small airway structure and function, we developed a strategy using fiberoptic bronchoscopy and brushing to sample the human small airway (10th-12th order) bronchial epithelium to assess gene expression (HG-133 Plus 2.0 array) in phenotypically normal smokers (n=10, 33 ± 7 pack-yr) compared to matched non-smokers (n=12). Even though the smokers were phenotypically normal, analysis of the small airway epithelium of the smokers compared to the non-smokers demonstrated up- and -down-regulation of genes in multiple categories relevant to the pathogenesis of chronic obstructive lung disease (COPD), including genes coding for cytokines/innate immunity, apoptosis, mucin, response to oxidants and xenobiotics, and general cellular processes. In the context that COPD starts in the small airways, these gene expression changes in the small airway epithelium in phenotypically normal smokers are candidates for the development of therapeutic strategies to prevent the onset of COPD. Keywords: smokers vs non-smokers
2006-11-21 | GSE4498 | GEO