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A muco-inflammatory milieu characterizes early cf lung disease

ABSTRACT: A muco-inflammatory milieu characterizes early cf lung disease

PROVIDER: PRJEB22216 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2098720_1.fastq.gz	Fastqsanger.gz
	ERR2098720_2.fastq.gz	Fastqsanger.gz
	ERR2098730_1.fastq.gz	Fastqsanger.gz
	ERR2098730_2.fastq.gz	Fastqsanger.gz
	ERR2098740_1.fastq.gz	Fastqsanger.gz

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Project description:A Muco-Inflammatory Milieu Characterizes Early CF Lung Disease

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A Muco-Inflammatory Milieu Characterizes Early CF Lung Disease

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Muco-Obstructive Lung Disease Exhibits Distinct Hypoxic and Inflammatory Airway Epithelial Gene Pathways

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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Gene expression in CF-vs-non CF human airway epithelial cell samples obtained by nasal brushing.

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Project description:Lung diseases, such as cystic fibrosis and COPD, are characterized by mucus obstruction and chronic airway inflammation, but their mechanistic link remains poorly understood. Here, we focused on the role of the mucostatic airway microenvironment on epigenetic reprogramming of airway macrophages (AM) and resulting transcriptomic and phenotypical changes. Using a muco-obstructive mouse model (Scnn1b-transgenic), we identified epigenetically controlled, differentially regulated pathways and transcription factors involved in inflammatory responses and macrophage polarization. Ex vivo stimulation of wild-type AMs with mucus induced gene expression changes, comparable with those observed in AMs from Scnn1b-transgenic mice. Functionally, AMs from Scnn1b-transgenic mice displayed impaired efferocytosis, phagocytosis and excessive inflammatory responses upon lipopolysaccharide challenge, mediated through enhanced Irf1 activity and expression. Our data show that mucostasis induces epigenetic reprogramming of AMs, leading to changes favoring tissue damage and disease progression. Targeting of these altered AMs may support therapeutic approaches in patients with muco-obstructive lung diseases.

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