Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells.
Christian HerrKonstantinos TsitourasJulia NiederstraßerChristina BackesChristoph BeisswengerLi DongLoïc GuillotAndreas KellerRobert BalsPublished in: Respiratory research (2020)
The transcriptome patterns of host defense and inflammatory genes are significantly distinct between ECIG-exposed and TCIG-treated cells. The overall effects of ECIGs on epithelial cells are less in comparison to TCIG, and ECIG-vapor does not affect host defense. Nevertheless, although acute exposure to ECIG-vapor induces inflammation, and the expression of S100 proteins, long term in vivo data is needed to evaluate the chronic effects of ECIG use.
Keyphrases
- oxidative stress
- induced apoptosis
- genome wide
- poor prognosis
- liver failure
- cell cycle arrest
- drug induced
- respiratory failure
- innate immune
- smoking cessation
- single cell
- gene expression
- rna seq
- electronic health record
- big data
- dna methylation
- aortic dissection
- hepatitis b virus
- transcription factor
- long non coding rna
- genome wide identification
- cell proliferation
- extracorporeal membrane oxygenation
- data analysis