Human lung metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA235284 | ENA |
REPOSITORIES: ENA
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Project description:Intraluminal obstruction produces chronic airway epithelial hypoxia. We investigated how chronic airway epithelial hypoxia and inflammatory stimuli interact in human bronchial epithelial (HBE) cultures and resected human bronchiectatic lungs to produce the diseased epithelial environment characteristic of muco-obstructive diseases. HBE cultures were exposed to normoxia or hypoxia (1% O₂) for 4 days, and concurrently treated with supernatants from cystic fibrosis (CF) lung-derived mucopurulent material (SMM) or PBS for 5 days. Bulk RNA-sequencing was perfomed. Results: Hypoxia and SMM regulated largely separate transcriptional programmes regardless of treatment order. PTGS2 (COX2) and CCL20 represented a small number of genes additively upregulated by both hypoxia and SMM. Conclusion: Chronic hypoxia and inflammation regulated distinct genes/pathways that combine to produce complex diseased environments in muco-obstructed airways.
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Project description:Intraluminal obstruction produces chronic airway epithelial hypoxia. We investigated how chronic airway epithelial hypoxia and inflammatory stimuli (supernatatants of mucopurulent materials: SMM) interact in human bronchial epithelial (HBE) cultures and resected bronchiectatic lungs to produce the diseased epithelial environment characteristic of muco-obstructive diseases. Results: Hypoxia and supernatants of mucopurulent materials (SMM) regulated largely separate transcriptional programmes regardless of treatment order. PTGS2 and CXCL8 represented a small number of genes additively upregulated by both hypoxia and SMM. HIF1A knockdown and EPAS1 knockdown produced distinct, often opposing, effects on hypoxia-responsive pathways. HIF1A dominated upregulation of glycolytic pathway signalling. EPAS1 regulated genes that increase mucus concentration under hypoxia (e.g., SCNN1G). Conclusion: Chronic hypoxia and inflammation regulated distinct genes/pathways that combine to produce complex diseased environments in muco-obstructed airways. HIF1α and EPAS1 regulated distinct hypoxia-induced transcriptional responses.
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