This SuperSeries is composed of the SubSeries listed below.
Peripheral blood gene expression changes during allergen inhalation challenge in atopic asthmatic individuals.
Sex, Age, Specimen part
View SamplesTo determine differential gene expression in peripheral blood of asthmatic individuals undergoing allergen inhalation challenge, post-challenge compared to pre-challenge
Peripheral blood gene expression changes during allergen inhalation challenge in atopic asthmatic individuals.
Sex, Age, Specimen part
View SamplesDetecting differential changes in the peripheral whole-blood transcriptome, post-challenge compared to pre-challenge; using non-globin reduced PAXgene (PAX.NGR) tubes
Peripheral blood gene expression changes during allergen inhalation challenge in atopic asthmatic individuals.
Sex, Age, Specimen part
View SamplesDetecting differential changes in the peripheral whole-blood transcriptome, post-challenge compared to pre-challenge; using globin reduced PAXgene (PAX.GR) tubes
Peripheral blood gene expression changes during allergen inhalation challenge in atopic asthmatic individuals.
Sex, Age, Specimen part
View SamplesLung cancers are documented to have remarkable intratumoral genetic heterogeneity. However, little is known about the heterogeneity of biophysical properties, such as cell motility, and its relationship to early disease pathogenesis and micrometastatic dissemination. In this study, we identified and selected a subpopulation of highly migratory premalignant pulmonary epithelial cells that were observed to migrate through microscale constrictions at up to 100-fold the rate of unselected cells. This enhanced migratory capacity was found to be Rac1-dependent and heritable, as evidenced by maintenance of the phenotype through multiple cell divisions continuing more than 8-weeks post-selection. The morphology of this lung epithelial subpopulation was characterized by increased cell protrusion intensity. In a murine model of micrometastatic seeding and pulmonary colonization, the motility-selected premalignant cells exhibit both enhanced survival in short term assays and enhanced outgrowth of premalignant lesions in longer term assays, thus overcoming important aspects of metastatic inefficiency. Overall, our findings indicate that among premalignant pulmonary epithelial cells, subpopulations with heritable motility-related biophysical properties exist, and these may explain micrometastatic seeding occurring early in the pathogenesis of lung cancer. Understanding, targeting, and preventing these critical biophysical traits and their underlying molecular mechanisms may provide a new approach to prevent metastatic behavior.
Identification of a Human Airway Epithelial Cell Subpopulation with Altered Biophysical, Molecular, and Metastatic Properties.
Age, Specimen part
View SamplesRNA sequencing was performed on RNA isolated from baseline biopsies from UC patients enrolled in the Phase II EUCALYPTUS study of etrolizumab. Gene expression differences were identified in a subset of anti-TNF naïve patients that achieved clinical remission at 10 weeks in response to etrolizumab. Overall design: Baseline colonic biopsies from UC patients treated with etrolizumab were sequenced by the Illumina HiSeq 2000 Sequencing System.
Association Between Response to Etrolizumab and Expression of Integrin αE and Granzyme A in Colon Biopsies of Patients With Ulcerative Colitis.
No sample metadata fields
View SamplesBackground: The first step in SARS-CoV-2 infection is binding of the virus to angiotensin converting enzyme 2 (ACE2) on the airway epithelium. Asthma affects over 300 million people world-wide, many of whom may encounter SARS-CoV-2. Epidemiologic data suggests that asthmatics who get infected may be at increased risk of more severe disease. Our objective was to assess whether maintenance inhaled corticosteroids (ICS), a major treatment for asthma, is associated with airway ACE2 expression in asthmatics.
Up-regulation of ACE2, the SARS-CoV-2 receptor, in asthmatics on maintenance inhaled corticosteroids.
Specimen part, Treatment
View SamplesAirway remodelling in chronic obstructive pulmonary disease (COPD) originates, in part, from smoking-induced changes in airway basal stem/progenitor cells (BCs). Based on the knowledge that bone morphogenetic protein 4 (BMP4) influences epithelial progenitor function in the developing and adult mouse lung, we hypothesised that BMP4 signalling may regulate the biology of adult human airway BCs relevant to COPD.
Expression of the SARS-CoV-2 ACE2 Receptor in the Human Airway Epithelium.
Specimen part
View SamplesEpidemiological studies have demonstrated that exposure to particulate matter (PM) ambient pollution has adverse effects on lung health, exacerbated by cigarette smoking. Fine airborne particles <2.5 m (PM2.5) are the most harmful of the urban pollutants, and the most closely linked to respiratory disease. Based on the knowledge that the small airway epithelium (SAE) plays a central role in pathogenesis of smoking-related lung disease, we hypothesized that elevated PM2.5 levels are associated with dysregulation of SAE gene expression.
Ambient Pollution-related Reprogramming of the Human Small Airway Epithelial Transcriptome.
Specimen part
View SamplesBackground: Metabolic plasticity involving shifts between mitochondrial respiration and glycolysis is emerging as a crucial component of efficient innate immune cell responses. Alveolar macrophages (AMs), the most abundant antigen-presenting cells in the lung, are dramatically increased in the lungs of patients with chronic obstructive pulmonary disease (COPD). However, COPD AMs exhibit dysfunctional responses to infection with lower phagocytic ability and impairment of mitochondrial reactive oxygen species (ROS) generation. Little is known about the mitochondrial function or respiration of these cells and whether alterations in their mitochondrial or glycolytic activities may contribute to the pathogenesis of COPD.
Alveolar Macrophage Immunometabolism and Lung Function Impairment in Smoking and Chronic Obstructive Pulmonary Disease.
Sex, Age, Specimen part, Race
View Samples