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Decipher immune response in early recovery phase of respiratory virus-induced disorder [BAL scRNA-seq]

ABSTRACT: Decipher immune response in early recovery phase of respiratory virus-induced disorder [BAL scRNA-seq]

PROVIDER: PRJNA1024518 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26297416.fastq.gz	Fastqsanger.gz
	SRR28705038_1.fastq.gz	Fastqsanger.gz
	SRR28705038_2.fastq.gz	Fastqsanger.gz

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Decipher immune response in early recovery phase of respiratory virus-induced disorder

Project description:Decipher immune response in early recovery phase of respiratory virus-induced disorder

| PRJNA1024517 | ENA

Decipher immune response in early recovery phase of respiratory virus-induced disorder [BAL scRNA-seq]

Project description:Appropriate lung repair responses are essential to restore functional integrity and prevent severe disease phenotypes after injury. While macrophages are thought to contribute to repair, whether distinct subsets occupy particular niches and assume dedicated tasks to mediate host recovery post- injury remains unknown. Using an in vivo model of influenza A virus (IAV) infection in combination with single-cell and spatial transcriptomic analyses, bone marrow chimeras and monocyte fate-mapping, we found the transitional appearance of Ccr2-dependent monocyte-derived Ly6G+ macrophages (Ly6G Macs) after viral clearance. Ly6G Macs inhabited the alveolar spaces of regenerating perilesional areas, exhibited a unique ultrastructural morphology as well as a high metabolic potential. Using in vivo gene targeting and ex vivo wound healing assays, we found that Ly6G Macs could limit disease severity and promote alveolar regeneration via interleukin-4 receptor- and arginase-1-dependent mechanisms acting on type 2 alveolar epithelial cells. We also found evidence that similar macrophages existed in other models of lung injury and in the airways of virally-infected humans. Our study thus identifies perilesional alveolar Ly6G Macs as a spatially-restricted short-lived macrophage subset engaging a crosstalk with type 2 alveolar epithelial cells to promote alveolar regeneration and recovery post-injury, thus representing an attractive therapeutic target.

2024-05-30 | GSE244764 | GEO

Decipher immune response in early recovery phase of respiratory virus-induced disorder [Ly6GMacs scRNA-seq]

Project description:Decipher immune response in early recovery phase of respiratory virus-induced disorder [Ly6GMacs scRNA-seq]

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Decipher immune response in early recovery phase of respiratory virus-induced disorder

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HLA-DR peptides from human BAL and EBV-transformed B cells

Project description:Optimization of the protocols for isolation HLA-DR (MHCII) peptides from human BAL.

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Patient-derived airway organoids from BAL fluid model injury and therapy responses in neonatal bronchopulmonary dysplasia [BAL Organoids Single Cell]

Project description:Lung tissue from fetal and neonatal lung samples is tough to obtain, and capturing cells from a living patient with evolving or established disease is very challenging. We hypothesized that airway organoids derived from BAL samples from intubated preterm neonates with established BPD will recapitulate the epithelial heterogeneity seen in human airways and can be used for studying injury and therapy responses in vitro. BPD patient BAL-derived airway organoids exhibited cellular heterogeneity consistent with that observed in the human airway. BAL sample-derived airway organoids from patients with established BPD contain basal cell progenitors and a spectrum of differentiated epithelial subtypes, including secretory, ciliated, PNECs, and hillock cells. Hyperoxia exposure and treatment with dexamethasone caused significant cellular transcriptional changes and highlighted biological pathways, both known and novel. Sex as a biological variable modulates the response of the BAL-derived airway organoid to hyperoxia exposure and treatment with dexamethasone. We also validated our findings in an independent dataset from human BPD lung samples. BAL-derived human lung organoids represent a cutting-edge model that bridges a critical gap in BPD research. They combine the advantages of being patient-specific and capturing developmental lung biology, with the experimental flexibility of an in vitro system.

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