Ontology highlight
ABSTRACT:
PROVIDER: PRJNA553808 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9685472_1.fastq.gz | Fastqsanger.gz | |||
| SRR9685472_2.fastq.gz | Fastqsanger.gz |
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Project description:Exposure to cigarette smoke (CS) is etiologically linked to the development of fatal respiratory diseases, and there is a need to understand the mechanisms whereby CS causes damage. While animal models have provided valuable insights into smoking-related respiratory tract damage, modern toxicity testing calls for reliable in vitro models as alternatives for animal experimentation. Primary cells and immortalized cell lines can be used to gain some insight; however, the three-dimensional organotypic culture systems probably better mimic the morphological, physiological, and molecular attributes of the human respiratory tract. Even though the bronchus, bronchioles, and lung parenchyma are the primary sites of smoking-related respiratory disease manifestation, the nasal epithelium has been proposed as a surrogate tissue to study the effects of smoking on the respiratory tract. Here, we report on a repeated whole mainstream CS exposure of nasal and bronchial organotypic tissue cultures from which transcriptomic data were collected at several post-exposure time points. Despite the remarkably similar histology and cellular response to whole CS in both tissue types, as measured by cellular staining and cytokine secretion assessment, transcriptomic analyses combined with quantitative biological network modeling identified biological mechanisms that were unique to bronchial tissue at late post-exposure time points. Organotypic models therefore appear to be a promising alternative to animal experimentation, and provide species-relevant insights into the effects of CS exposure on the respiratory system.
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Project description:Respiratory syncytial virus (RSV) is a seasonal respiratory pathogen that primarily affects young children, potentially causing severe lower respiratory tract disease. Despite the high disease burden, understanding of RSV pathophysiology remains limited. To address this, advanced RSV infection models are needed. While HEp-2 cells are widely used due to their high susceptibility to RSV, they do not accurately reflect the host response of the human respiratory tract. In this study, we evaluated human induced pluripotent stem cell-derived respiratory organoids, which contain respiratory epithelial cells, immune cells, fibroblasts, and vascular endothelial cells, for their potential to model RSV infection and support pharmaceutical research. RSV-infected organoids exhibited high viral genome and protein expression, epithelial layer destruction, and increased collagen accumulation. Pro-inflammatory cytokine levels in culture supernatants also increased post-infection. Furthermore, RSV infection was significantly inhibited by monoclonal antibodies (nirsevimab, palivizumab, suptavumab, or clesrovimab), while ribavirin showed limited efficacy. These findings highlight the utility of respiratory organoids for RSV research.
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