The transcriptomic signature of respiratory sensitizers using an alveolar model.
Matthew GibbJames Y LiuChristie M SayesPublished in: Cell biology and toxicology (2024)
Environmental contaminants are ubiquitous in the air we breathe and can potentially cause adverse immunological outcomes such as respiratory sensitization, a type of immune-driven allergic response in the lungs. Wood dust, latex, pet dander, oils, fragrances, paints, and glues have all been implicated as possible respiratory sensitizers. With the increased incidence of exposure to chemical mixtures and the rapid production of novel materials, it is paramount that testing regimes accounting for sensitization are incorporated into development cycles. However, no validated assay exists that is universally accepted to measure a substance's respiratory sensitizing potential. The lungs comprise various cell types and regions where sensitization can occur, with the gas-exchange interface being especially important due to implications for overall lung function. As such, an assay that can mimic the alveolar compartment and assess sensitization would be an important advance for inhalation toxicology. Some such models are under development, but in-depth transcriptomic analyses have yet to be reported. Understanding the transcriptome after sensitizer exposure would greatly advance hazard assessment and sustainability. We tested two known sensitizers (i.e., isophorone diisocyanate and ethylenediamine) and two known non-sensitizers (i.e., chlorobenzene and dimethylformamide). RNA sequencing was performed in our in vitro alveolar model, consisting of a 3D co-culture of epithelial, macrophage, and dendritic cells. Sensitizers were readily distinguishable from non-sensitizers by principal component analysis. However, few differentially regulated genes were common across all pair-wise comparisons (i.e., upregulation of genes SOX9, UACA, CCDC88A, FOSL1, KIF20B). While the model utilized in this study can differentiate the sensitizers from the non-sensitizers tested, further studies will be required to robustly identify critical pathways inducing respiratory sensitization.
Keyphrases
- solar cells
- single cell
- lung function
- dendritic cells
- rna seq
- genome wide
- respiratory tract
- high throughput
- immune response
- transcription factor
- cystic fibrosis
- chronic obstructive pulmonary disease
- emergency department
- stem cells
- gene expression
- air pollution
- risk factors
- human health
- mesenchymal stem cells
- metabolic syndrome
- poor prognosis
- adipose tissue
- signaling pathway
- drinking water
- dna methylation
- skeletal muscle
- cell proliferation
- genome wide identification
- health risk assessment
- bioinformatics analysis
- long non coding rna
- drug induced