E-GEOD-36906
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA157321PRJNA126737
PROVIDER: E-GEOD-36906 | ExpressionAtlas | 2015-09-28
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-36906-analysis-methods.tsv | Tabular | |||
| E-GEOD-36906-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-36906-configuration.xml | Xml | |||
| E-GEOD-36906-percentile-ranks.tsv | Tabular | |||
| E-GEOD-36906.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 46 |
Similar Datasets
Project description:Cystic fibrosis (CF) is a life-shortening disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Although bacterial lung infection and the resulting inflammation cause most of the morbidity and mortality, how loss of CFTR first disrupts airway host defense has remained uncertain. We asked what abnormality impairs elimination when a bacterium lands on the pristine surface of a newborn CF airway? To investigate this defect, we interrogated the viability of individual bacteria immobilized on solid grids and placed on the airway surface. As a model we studied CF pigs, which spontaneously develop hallmark features of CF lung disease. At birth, their lungs lack infection and inflammation, but have a reduced ability to eradicate bacteria. Here we show that in newborn wild-type pigs, the thin layer of airway surface liquid (ASL) rapidly killed bacteria in vivo, when removed from the lung, and in primary epithelial cultures. Lack of CFTR reduced bacterial killing. We found that ASL pH was more acidic in CF, and reducing pH inhibited the antimicrobial activity of ASL. Reducing ASL pH diminished bacterial killing in wild-type pigs, and increasing ASL pH rescued killing in CF pigs. These results directly link the initial host defense defect to loss of CFTR, an anion channel that facilitates HCO3- transport. Without CFTR, airway epithelial HCO3- secretion is defective, ASL pH falls and inhibits antimicrobial function, and thereby impairs killing of bacteria that enter the newborn lung. These findings suggest that increasing ASL pH might prevent the initial infection in patients with CF and that assaying ASL pH or bacterial killing could report on the benefit of therapeutic interventions. 11 samples of trachea primary airway epithelial cultures representing CFTR+/+ and CFTR-/- pigs. Pig samples representing 14 bronchus and 12 trachea tissue samples submitted in GSE21071.
2012-03-29 | E-GEOD-36906 | biostudies-arrayexpress
Project description:Primary Human Airway Epithelial Cultures infected with SARS-CoV-2
2020-12-09 | E-GEOD-153970 | ExpressionAtlas
Project description:Cystic fibrosis (CF) is a life-shortening disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Although bacterial lung infection and the resulting inflammation cause most of the morbidity and mortality, how loss of CFTR first disrupts airway host defense has remained uncertain. We asked what abnormality impairs elimination when a bacterium lands on the pristine surface of a newborn CF airway? To investigate this defect, we interrogated the viability of individual bacteria immobilized on solid grids and placed on the airway surface. As a model we studied CF pigs, which spontaneously develop hallmark features of CF lung disease. At birth, their lungs lack infection and inflammation, but have a reduced ability to eradicate bacteria. Here we show that in newborn wild-type pigs, the thin layer of airway surface liquid (ASL) rapidly killed bacteria in vivo, when removed from the lung, and in primary epithelial cultures. Lack of CFTR reduced bacterial killing. We found that ASL pH was more acidic in CF, and reducing pH inhibited the antimicrobial activity of ASL. Reducing ASL pH diminished bacterial killing in wild-type pigs, and increasing ASL pH rescued killing in CF pigs. These results directly link the initial host defense defect to loss of CFTR, an anion channel that facilitates HCO3- transport. Without CFTR, airway epithelial HCO3- secretion is defective, ASL pH falls and inhibits antimicrobial function, and thereby impairs killing of bacteria that enter the newborn lung. These findings suggest that increasing ASL pH might prevent the initial infection in patients with CF and that assaying ASL pH or bacterial killing could report on the benefit of therapeutic interventions.
2012-03-30 | GSE36906 | GEO
Project description:Expression data from airway brush biopsy samples, differentiated primary cultures of human airway epithelia, CaLu3 cultures at the air liquid interface, and primary cultures of human airway epithelia submerged in nutrient media Organotypic cultures of primary human airway epithelial cells have been used to investigate the morphology, ion and fluid transport, innate immunity, transcytosis, infection, inflammation, signaling, cilia and repair functions of this complex tissue. However, we do not know how close these cultures resemble the epithelia in vivo. In this study, we examine the genome-wide expression profile of human airway epithelial cells in vivo obtained from brush biopsies of the trachea and bronchus of healthy volunteers and compare it to the expression profile of primary cultures of human airway epithelia grown at the air-liquid interface. For comparison we also investigate the expression profile of Calu3 cells grown at the air-liquid interface and primary cultures of human airway epithelia submerged in nutrient media. We compare the transcriptional profile of human in vivo airway epithelia from trachea and bronchus to differentiated primary human airway epithelia cultures, also from trachea and bronchus, and grown at the air-liquid interface. We also included the profile of Calu3 cultures grown at the air-liquid interface and primary cultures submerged in nutrient media.
2010-04-15 | E-GEOD-20502 | biostudies-arrayexpress
Project description:Expression data from airway brush biopsy samples, differentiated primary cultures of human airway epithelia, CaLu3 cultures at the air liquid interface, and primary cultures of human airway epithelia submerged in nutrient media Organotypic cultures of primary human airway epithelial cells have been used to investigate the morphology, ion and fluid transport, innate immunity, transcytosis, infection, inflammation, signaling, cilia and repair functions of this complex tissue. However, we do not know how close these cultures resemble the epithelia in vivo. In this study, we examine the genome-wide expression profile of human airway epithelial cells in vivo obtained from brush biopsies of the trachea and bronchus of healthy volunteers and compare it to the expression profile of primary cultures of human airway epithelia grown at the air-liquid interface. For comparison we also investigate the expression profile of Calu3 cells grown at the air-liquid interface and primary cultures of human airway epithelia submerged in nutrient media.
2010-04-15 | GSE20502 | GEO
Project description:Phenotypic responses of differentiated asthmatic human airway epithelial cultures to rhinovirus
2025-01-24 | E-GEOD-61141 | ExpressionAtlas
Project description:Gene expression profile of NRf knockout newborn rodents exposed to hyperoxia
2015-09-18 | E-GEOD-29632 | ExpressionAtlas
Project description:We did bulk RNA sequencing in newborn cystic fibrosis (CF) and non-CF pig kidney. We compared kidney gene expression profiling between non-CF and CF pigs. RNA sequencing results showed that there is not significant difference between non-CF and CF in terms of gene expression, suggesting that CFTR knockout does not affect kidney development in newborn pigs.
2024-06-07 | GSE217122 | GEO
Project description:Gene expression profile of SUMO knockout in human mammary epithelial cells
2025-01-24 | E-GEOD-34055 | ExpressionAtlas
Project description:Elexacaftor/tezacaftor/ivacaftor (ETI, Trikafta) is highly effective treatment for many cystic fibrosis patients, at least partly because it increases CFTR mediated Cl- and HCO3- secretion by airway epithelial cells leading to improved lung function and less frequent exacerbations and hospitalizations. However, little is known about how ETI affects airway epithelial cells in ways not related to CFTR mediated Cl- and HCO3- secretion, for example how ETI affects the expression of genes other than CFTR or how ETI might affect airway cells’ response to infection. It is established that CF airway cells bearing the delta F 508 mutation the CFTR gene respond characteristically differently from wild type CFTR cells, and we hypothesized that, as a highly effective CFTR modulator, ETI might make airway cells from CF donors respond to pathogen stimulation (Pseudomonas aeruginosa PA14 or outer membrane vesicles isolated from these bacteria) in more the same way that cells from wild type, healthy control cells do. We tested this hypothesis by measuring gene expression responses in polarized primary CF airway cells exposed to ETI alone or ETI in the presence of a pathogen challenge (PA14 or outer membrane vesicles). Responses of CFTR wild type primary CF airway cells to PA14 or outer membrane vesicles was also measured for comparison
2024-06-25 | GSE268718 | GEO