Electronic cigarette smoke reduces ribosomal protein gene expression to impair protein synthesis in primary human airway epithelial cells.

Introduction:
This text presents a scientific study on the effects of electronic cigarette (e-cig) smoke solution on primary human airway epithelial cells. The study identifies transcriptomic changes, including decreased expression of many ribosomal genes, and the impact on protein biogenesis in these cells. additionally, the study identifies several flavoring chemicals and dicarbonyls present in the e-cig smoke solution.

Key Points:

* The study used a TE-2B smoking machine to puff twenty e-cig cartridges and collected the downstream smoke through an impinger filled with ultrapure water to generate e-cig smoke solution.
* GC/MS analysis identified five flavoring chemicals designated as 'high priority' by a flavoring industry report on respiratory hazards associated with flavoring chemicals and the presence of methylglyoxal.
* Primary normal human bronchial epithelial (NhBE) cells were cultured at an air-liquid interface (aLI) and exposed to e-cig smoke solution for 24 hours.
* RNa-seq analysis identified over 200 differentially expressed genes in NhBE cells exposed to e-cig smoke solution.
* Exposure to e-cig smoke solution inhibits biological pathways involving ribosomes and protein biogenesis in NhBE cells.
* Expression of corresponding ribosomal proteins and subsequent protein biogenesis are reduced in the cells exposed to e-cig.
* The study suggests that e-cig smoke may perturb ribosomal functions and protein biogenesis, potentially contributing to lung injuries in e-cig users.

Main Message:
The study's findings suggest that e-cig smoke solution affects biological pathways related to ribosomal proteins and protein synthesis in NhBE cells. The reduction in ribosomal protein-encoding genes and new protein synthesis from the cells is a potential mechanism by which e-cig use may impact lung epithelium. Further studies are needed to evaluate the effects of e-cig on airway epithelium and how these changes contribute to the current epidemic of lung injuries in e-cig users. The study also highlights the need for further investigation into how the chemicals in e-cig smoke solution, including flavoring chemicals and dicarbonyls, may contribute to lung injuries.

Park hR, Vallarino J, O’Sullivan M, et al. Electronic cigarette smoke reduces ribosomal protein gene expression to impair protein synthesis in primary human airway epithelial cells. Scientific reports. 2021;11(1):17517. doi:10.1038/s41598-021-97013-z