Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA263957 | ENA |
REPOSITORIES: ENA
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Project description:Inhaled welding fumes are deposited on all parts of the respiratory system, with the nasal cavity being the initial point of contact. We investigated the influence of fresh welding fumes on nasal epithelial model, i.e., RPMI 2650 cells, at the transcriptome level. Spark-generated welding fumes at two different concentrations (85 µg/m3 - low; 760 µg/m3 - high) were exposed to RPMI 2650 cell monolayers at air-liquid-interface continuously for 6h, followed by zero hours (or) four hours post-exposure incubation.
2014-12-01 | GSE62384 | GEO
Project description:The respiratory epithelium is the body’s first line of defense to pathogens, pollutants, and other potentially injurious agents that can be inhaled. Sampling the upper respiratory tract is becoming a widely used technique in the clinic to examine the molecular changes in the diseased airway; however, it is unclear as to whether the responses in the upper respiratory tract (i.e. the nasal turbinates) reflect the changes that occur in the lower respiratory tract (i.e. trachea and lungs). Here, we assessed the responses to poly I:C, a synthetic double-stranded RNA molecule that is meant to mimic the acute effects of a viral infection, in both the upper and lower respiratory tracts of cynomolgus macaques. To do this, we compared the in vivo response after a nasal poly I:C challenge in a nasal scrape samples (performed using a nasal curette) to responses that occurred after ex vivo poly I:C stimulation in nasal scrapes, tracheal epithelial brushings, and lung tissue explants in non-human primates.
2015-10-11 | GSE41668 | GEO
Project description:The respiratory epithelium is the body’s first line of defense to pathogens, pollutants, and other potentially injurious agents that can be inhaled. Sampling the upper respiratory tract is becoming a widely used technique in the clinic to examine the molecular changes in the diseased airway; however, it is unclear as to whether the responses in the upper respiratory tract (i.e. the nasal turbinates) reflect the changes that occur in the lower respiratory tract (i.e. trachea and lungs). Here, we assessed the responses to poly I:C, a synthetic double-stranded RNA molecule that is meant to mimic the acute effects of a viral infection, in both the upper and lower respiratory tracts of cynomolgus macaques. To do this, we compared the in vivo response after a nasal poly I:C challenge in a nasal scrape samples (performed using a nasal curette) to responses that occurred after ex vivo poly I:C stimulation in nasal scrapes, tracheal epithelial brushings, and lung tissue explants in non-human primates.
2015-10-11 | GSE41670 | GEO
Project description:The respiratory epithelium is the body’s first line of defense to pathogens, pollutants, and other potentially injurious agents that can be inhaled. Sampling the upper respiratory tract is becoming a widely used technique in the clinic to examine the molecular changes in the diseased airway; however, it is unclear as to whether the responses in the upper respiratory tract (i.e. the nasal turbinates) reflect the changes that occur in the lower respiratory tract (i.e. trachea and lungs). Here, we assessed the responses to poly I:C, a synthetic double-stranded RNA molecule that is meant to mimic the acute effects of a viral infection, in both the upper and lower respiratory tracts of cynomolgus macaques. To do this, we compared the in vivo response after a nasal poly I:C challenge in a nasal scrape samples (performed using a nasal curette) to responses that occurred after ex vivo poly I:C stimulation in nasal scrapes, tracheal epithelial brushings, and lung tissue explants in non-human primates.
2015-10-11 | GSE41672 | GEO
Project description:The respiratory epithelium is the body’s first line of defense to pathogens, pollutants, and other potentially injurious agents that can be inhaled. Sampling the upper respiratory tract is becoming a widely used technique in the clinic to examine the molecular changes in the diseased airway; however, it is unclear as to whether the responses in the upper respiratory tract (i.e. the nasal turbinates) reflect the changes that occur in the lower respiratory tract (i.e. trachea and lungs). Here, we assessed the responses to poly I:C, a synthetic double-stranded RNA molecule that is meant to mimic the acute effects of a viral infection, in both the upper and lower respiratory tracts of cynomolgus macaques. To do this, we compared the in vivo response after a nasal poly I:C challenge in a nasal scrape samples (performed using a nasal curette) to responses that occurred after ex vivo poly I:C stimulation in nasal scrapes, tracheal epithelial brushings, and lung tissue explants in non-human primates.
2015-10-11 | GSE41671 | GEO
Project description:The respiratory epithelium is the body’s first line of defense to pathogens, pollutants, and other potentially injurious agents that can be inhaled. Sampling the upper respiratory tract is becoming a widely used technique in the clinic to examine the molecular changes in the diseased airway; however, it is unclear as to whether the responses in the upper respiratory tract (i.e. the nasal turbinates) reflect the changes that occur in the lower respiratory tract (i.e. trachea and lungs). Here, we assessed the responses to poly I:C, a synthetic double-stranded RNA molecule that is meant to mimic the acute effects of a viral infection, in both the upper and lower respiratory tracts of cynomolgus macaques. To do this, we compared the in vivo response after a nasal poly I:C challenge in a nasal scrape samples (performed using a nasal curette) to responses that occurred after ex vivo poly I:C stimulation in nasal scrapes, tracheal epithelial brushings, and lung tissue explants in non-human primates.
2015-10-11 | GSE41669 | GEO
Project description:Molecular profiling studies in asthma cohorts have identified a Th2-driven asthma subtype, characterized by elevated lower airway expression of POSTN, CLCA1 and SERPINB2. To assess upper airway gene expression as a potential biomarker for lower airway Th2 inflammation, we assayed upper airway (nasal) and lower airway (bronchial) epithelial gene expression, serum total IgE, blood eosinophils and serum periostin in a cohort of 54 allergic asthmatics and 30 matched healthy controls. 23 of 51 asthmatics in our cohort were classified as âTh2 highâ based on lower airway Th2 gene signature expression. Consistent with this classification, âTh2 highâ subjects displayed elevated total IgE and blood eosinophil levels relative to âTh2 lowâ subjects. Upper airway Th2 signature expression was significantly correlated with lower airway Th2 signature expression (r=0.44), with similar strength of association as serum total IgE and blood eosinophils, known biomarkers of Th2 inflammation. In an unbiased genome-wide scan, we identified 8 upper airway genes more strongly correlated with lower airway Th2 gene signature expression (r=0.58), including Eotaxin-3 (CCL26), Galectin-10 (CLC) and Cathepsin-C (CTSC). Asthmatics classified as âTh2 highâ using this 8-gene signature show similar serum total IgE and blood eosinophil levels as âTh2 highâ asthmatics classified using lower airway Th2 gene signature expression. We have identified an 8-gene upper airway signature correlated with lower airway Th2 inflammation, which may be used as a diagnostic biomarker for Th2-driven asthma. Upper airway (nasal) and lower airway (bronchial) epithelial brushings obtained from a cohort of 54 allergic asthmatics and 30 matched healthy controls were profiled by gene expression by microarray. Subjects were assayed for gene expression, serum total IgE, blood eosinophils and serum periostin.
2015-10-23 | E-GEOD-41861 | biostudies-arrayexpress
Project description:Rationale: Emerging evidence suggests that disease vulnerability is expressed throughout the airways; the so-called “unified airway hypothesis” but the evidence to support this is predominantly indirect. Objectives: To establish the transcriptomic profiles of the upper and lower airway and determine their level of similarity irrespective of airway symptoms (wheeze) and allergy. Methods: We performed RNA-sequencing on upper and lower airway epithelial cells from 63 children with or without wheeze and accompanying atopy, utilizing differential gene expression and gene co-expression analyses to determine transcriptional similarity. Results: We observed ~91% homology in the expressed between the two sites. When co-expressed genes were grouped into modules relating to biological functions, all were found to be conserved between the two regions, resulting in a consensus network containing 16 modules associated with ribosomal function, metabolism, gene expression, mitochondrial activity and anti-viral responses through interferon activity. Although symptom associated gene expression changes were more prominent in the lower airway, they were reflected in nasal epithelium and included; IL1RL1, PTGS1, CCL26 and POSTN. Through network analysis we identified a cluster of co-expressed genes associated with atopic-wheeze in the lower airway, which could equally distinguish atopic and non-atopic phenotypes in upper airway samples. Conclusions: We show that the upper and lower airway are significantly conserved in their transcriptional composition, and that variations associated with disease are present in both nasal and tracheal epithelium. Clinical Implication: Findings from this study supporting a unified airway imply that clinical insight regarding the lower airway in health and disease can be gained from studying the nasal epithelium.
2020-03-05 | GSE118761 | GEO
Project description:Molecular profiling studies in asthma cohorts have identified a Th2-driven asthma subtype, characterized by elevated lower airway expression of POSTN, CLCA1 and SERPINB2. To assess upper airway gene expression as a potential biomarker for lower airway Th2 inflammation, we assayed upper airway (nasal) and lower airway (bronchial) epithelial gene expression, serum total IgE, blood eosinophils and serum periostin in a cohort of 54 allergic asthmatics and 30 matched healthy controls. 23 of 51 asthmatics in our cohort were classified as ‘Th2 high’ based on lower airway Th2 gene signature expression. Consistent with this classification, ‘Th2 high’ subjects displayed elevated total IgE and blood eosinophil levels relative to ‘Th2 low’ subjects. Upper airway Th2 signature expression was significantly correlated with lower airway Th2 signature expression (r=0.44), with similar strength of association as serum total IgE and blood eosinophils, known biomarkers of Th2 inflammation. In an unbiased genome-wide scan, we identified 8 upper airway genes more strongly correlated with lower airway Th2 gene signature expression (r=0.58), including Eotaxin-3 (CCL26), Galectin-10 (CLC) and Cathepsin-C (CTSC). Asthmatics classified as ‘Th2 high’ using this 8-gene signature show similar serum total IgE and blood eosinophil levels as ‘Th2 high’ asthmatics classified using lower airway Th2 gene signature expression. We have identified an 8-gene upper airway signature correlated with lower airway Th2 inflammation, which may be used as a diagnostic biomarker for Th2-driven asthma.
2015-10-23 | GSE41861 | GEO
Project description:Genetic variations at the 17q21 asthma-risk locus regulate the expression of gasdermin B (GSDMB) and ORMDL3, influencing inflammatory responses and sphingolipid metabolism. While asthma-associated 17q21 variations are known to affect ORMDL3 expression in immune and airway smooth muscle cells, its role in airway epithelial sphingolipid metabolism remains unclear. We investigated whether asthma and 17q21 genetic variations influence sphingolipid composition in the upper respiratory tract and how immune vs. epithelial cells contribute to this process. Sphingolipid profiles were analyzed in nasal fluid and blood from children with and without asthma. We also examined gene expression and sphingolipid composition in nasal epithelial cells and PBMCs from healthy adults homozygous for the rs7216389 C/C and T/T (asthma-risk) genotypes. Children with atopic asthma exhibited lower nasal fluid sphingolipids, including sphinganine, dihydroceramides, and ceramides, independent of corticosteroid use or allergic rhinitis. Asthma was further associated with higher plasma sphingolipids and lower blood cell sphingolipids, the latter mirroring patterns in nasal fluid. In PBMCs, the T allele increased ORMDL3 expression, suppressing de novo sphingolipid synthesis. However, in nasal epithelial cells, the T allele mainly increased GSDMB and there was no effect on sphingolipid metabolism. These findings establish nasal fluid sphingolipid profiling as a potential marker for atopic asthma and provide evidence of a cell-type-specific effect of 17q21 genetic variants. While ORMDL3-mediated sphingolipid suppression occurs in PBMCs and not airway epithelial cells, its systemic effects may contribute to lower airway sphingolipids in asthma.
2026-05-03 | GSE297032 | GEO