Methyl-Seq of Pediatric ARDS Nasal and Bronchial Brushings
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ABSTRACT:
PROVIDER: PRJNA793833 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The objective of this study was to determine if nasal transcriptomics could be used to characterize the underlying pathobiology and predict clinical course of patients with pediatric ARDS (PARDS). Subjects meeting consensus PARDS criteria or controls admitted to the Pediatric ICU without lung disease had nasal cytology brushings on days 1, 3, 7 and 14. The gene expression of these brushings was compared to identify subtypes and describe clinical course. Concurrent nasal and bronchial brushings were collected if bronchoscopy was performed. We identified four PARDS subgroups, termed A, B, C, and D. Subgroup B was marked by inflammation and ciliary cell dysfunction. Subgroup D was marked by reduced epithelial stem cell mRNAs without inflammation. Subgroup A had hypo-inflammation and upregulation of pathways important in epithelial cell repair. Subgroup C had increased ciliary cell genes. Control specimens almost entirely clustered with Subgroup C, but one that developed PARDS clustered with Subgroup B and several that developed lung injury clustereced with Subgroups B and A. Over time, Subgroups D and B transitioned to A which transitioned to C. Bronchial and nasal gene expresison were similar.
2021-12-24 | GSE192364 | GEO
Project description:NextGeneration Sequencing of Pediatric ARDS Nasal and Bronchial Brushings
| PRJNA791297 | ENA
Project description:The objective of this study was to identify differences in the nasal methylome of patients with Pediatric ARDS (PARDS) compared to controls and to observe how this might change over time. We found two different methylomic patterns. Subgroup 1 was comprised of entirely of PARDS subjects, and Subgroup 2 contained both control and PARDS subject. Subgroup 1was characterized by hypomethylation of genes related to cell adhesion and hypermethylation of cell metabolism-related genes. Over time, the methylation pattern of PARDS subjects changed, but the pattern of control subjects was stable. Five concurrent bronchial and nasal specimens were obtained showing very few differences in methylation between these two collection sites.
2022-01-06 | GSE192926 | GEO
Project description:This study used nasal transcriptomic profiling of the inferior turbinate in control and pediatric ARDS subjects to identify endotypes. This data set is for amplified specimens. The study identfied three pediatric ARDS endotypes.
2020-06-23 | GSE152979 | GEO
Project description:This study used nasal transcriptomic profiling of the inferior turbinate in control and pediatric ARDS subjects to identify endotypes. This data set is for non-amplified specimens. The study identfied three pediatric ARDS endotypes.
2020-06-23 | GSE152978 | GEO
Project description:SARS-CoV-2 infection and disease severity are influenced by viral entry (VE) gene expression patterns in the airway epithelium. The similarities and differences of VE gene expression (ACE2, TMPRSS2, and CTSL) across nasal and bronchial compartments have not been fully characterized using matched samples from large cohorts. Gene expression data from 793 nasal and 1673 bronchial brushes obtained from individuals participating in lung cancer screening or diagnostic workup revealed that smoking status (current versus former) was the only clinical factor significantly and reproducibly associated with VE gene expression. The expression of ACE2 and TMPRSS2 was higher in smokers in the bronchus but not in the nose. AQ1 scRNA-seq of nasal brushings indicated that ACE2 co-expressed genes were highly expressed in club and C15orf48 secretory cells while TMPRSS2 co-expressed genes were highly expressed in keratinizing epithelial cells. In contrast, these ACE2 and TMPRSS2 modules were highly expressed in goblet cells in scRNA-seq from bronchial brushings. Cell-type deconvolution of the gene expression data confirmed that smoking increased the abundance of several secretory cell populations in the bronchus, but only goblet cells in the nose. The association of ACE2 and TMPRSS2 with smoking in the bronchus is due to their high expression in goblet cells which increase in abundance in current smoker airways. In contrast, in the nose, these genes are not predominantly expressed in cell populations modulated by smoking. In individuals with elevated lung cancer risk, smokinginduced VE gene expression changes in the nose likely have minimal impact on SARS-CoV-2 infection, but in the bronchus, smoking may lead to higher viral loads and more severe disease.
2022-10-25 | GSE210695 | GEO
Project description:SARS-CoV-2 infection and disease severity are influenced by viral entry (VE) gene expression patterns in the airway epithelium. The similarities and differences of VE gene expression (ACE2, TMPRSS2, and CTSL) across nasal and bronchial compartments have not been fully characterized using matched samples from large cohorts. Gene expression data from 793 nasal and 1673 bronchial brushes obtained from individuals participating in lung cancer screening or diagnostic workup revealed that smoking status (current versus former) was the only clinical factor significantly and reproducibly associated with VE gene expression. The expression of ACE2 and TMPRSS2 was higher in smokers in the bronchus but not in the nose. AQ1 scRNA-seq of nasal brushings indicated that ACE2 co-expressed genes were highly expressed in club and C15orf48 secretory cells while TMPRSS2 co-expressed genes were highly expressed in keratinizing epithelial cells. In contrast, these ACE2 and TMPRSS2 modules were highly expressed in goblet cells in scRNA-seq from bronchial brushings. Cell-type deconvolution of the gene expression data confirmed that smoking increased the abundance of several secretory cell populations in the bronchus, but only goblet cells in the nose. The association of ACE2 and TMPRSS2 with smoking in the bronchus is due to their high expression in goblet cells which increase in abundance in current smoker airways. In contrast, in the nose, these genes are not predominantly expressed in cell populations modulated by smoking. In individuals with elevated lung cancer risk, smokinginduced VE gene expression changes in the nose likely have minimal impact on SARS-CoV-2 infection, but in the bronchus, smoking may lead to higher viral loads and more severe disease.
2022-10-25 | GSE210660 | GEO
Project description:SARS-CoV-2 infection and disease severity are influenced by viral entry (VE) gene expression patterns in the airway epithelium. The similarities and differences of VE gene expression (ACE2, TMPRSS2, and CTSL) across nasal and bronchial compartments have not been fully characterized using matched samples from large cohorts. Gene expression data from 793 nasal and 1673 bronchial brushes obtained from individuals participating in lung cancer screening or diagnostic workup revealed that smoking status (current versus former) was the only clinical factor significantly and reproducibly associated with VE gene expression. The expression of ACE2 and TMPRSS2 was higher in smokers in the bronchus but not in the nose. AQ1 scRNA-seq of nasal brushings indicated that ACE2 co-expressed genes were highly expressed in club and C15orf48 secretory cells while TMPRSS2 co-expressed genes were highly expressed in keratinizing epithelial cells. In contrast, these ACE2 and TMPRSS2 modules were highly expressed in goblet cells in scRNA-seq from bronchial brushings. Cell-type deconvolution of the gene expression data confirmed that smoking increased the abundance of several secretory cell populations in the bronchus, but only goblet cells in the nose. The association of ACE2 and TMPRSS2 with smoking in the bronchus is due to their high expression in goblet cells which increase in abundance in current smoker airways. In contrast, in the nose, these genes are not predominantly expressed in cell populations modulated by smoking. In individuals with elevated lung cancer risk, smokinginduced VE gene expression changes in the nose likely have minimal impact on SARS-CoV-2 infection, but in the bronchus, smoking may lead to higher viral loads and more severe disease.
2022-10-25 | GSE210659 | GEO
Project description:SARS-CoV-2 infection and disease severity are influenced by viral entry (VE) gene expression patterns in the airway epithelium. The similarities and differences of VE gene expression (ACE2, TMPRSS2, and CTSL) across nasal and bronchial compartments have not been fully characterized using matched samples from large cohorts. Gene expression data from 793 nasal and 1673 bronchial brushes obtained from individuals participating in lung cancer screening or diagnostic workup revealed that smoking status (current versus former) was the only clinical factor significantly and reproducibly associated with VE gene expression. The expression of ACE2 and TMPRSS2 was higher in smokers in the bronchus but not in the nose. AQ1 scRNA-seq of nasal brushings indicated that ACE2 co-expressed genes were highly expressed in club and C15orf48 secretory cells while TMPRSS2 co-expressed genes were highly expressed in keratinizing epithelial cells. In contrast, these ACE2 and TMPRSS2 modules were highly expressed in goblet cells in scRNA-seq from bronchial brushings. Cell-type deconvolution of the gene expression data confirmed that smoking increased the abundance of several secretory cell populations in the bronchus, but only goblet cells in the nose. The association of ACE2 and TMPRSS2 with smoking in the bronchus is due to their high expression in goblet cells which increase in abundance in current smoker airways. In contrast, in the nose, these genes are not predominantly expressed in cell populations modulated by smoking. In individuals with elevated lung cancer risk, smokinginduced VE gene expression changes in the nose likely have minimal impact on SARS-CoV-2 infection, but in the bronchus, smoking may lead to higher viral loads and more severe disease.
2022-10-25 | GSE210694 | GEO
Project description:The nasal and bronchial epithelium are unified parts of the respiratory tract that are affected in the monogenic disorder cystic fibrosis (CF). Recent studies have uncovered that nasal and bronchial tissues exhibit intrinsic variability, including differences in mucociliary cell composition and expression of unique transcriptional regulatory proteins which relate to germ layer origin. In the present study, we explored transcriptomic differences between cultured nasal and bronchial epithelial cells from people with CF. Comparison of air-liquid interface-differentiated epithelial cells from subjects with CF revealed distinct mucociliary differentiation states of nasal and bronchial cultures. Moreover, using RNA sequencing we identified cell type-specific signature transcription factors in differentiated nasal and bronchial epithelial cells.
2023-11-21 | GSE241801 | GEO