Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells

Area of Science:

• Cellular Biology
• Toxicology
• Respiratory Medicine

Background:

• Increasing use of electronic cigarettes (ECIGs) necessitates understanding their cellular impact.
• Limited knowledge exists on ECIG vapor effects on inflammation and host defense mechanisms.

Purpose of the Study:

• Compare acute effects of ECIG vapor and traditional cigarette (TCIG) smoke.
• Investigate impacts on host defense, inflammation, and cellular activation in airway epithelial cells.

Main Methods:

• Exposed primary human airway epithelial cells (pHBEs) and cell lines to ECIG vapor and TCIG smoke.
• Assessed epithelial host defense, barrier integrity, and gene expression via arrays and qRT-PCR.

Main Results:

• ECIG vapor did not affect bacterial killing, barrier integrity, or antimicrobial peptides compared to controls.
• TCIGs significantly impaired host defense and barrier integrity.
• ECIG exposure induced IL-8 in Calu-3 cells but not other cell types; gene expression profiles differed between ECIG and TCIG groups.

Conclusions:

• Transcriptome patterns for host defense and inflammatory genes differ significantly between ECIG and TCIG exposure.
• ECIGs have a lesser overall effect on epithelial cells than TCIGs; ECIG vapor does not impair host defense.
• Acute ECIG exposure induces inflammation and S100 protein expression, but long-term in vivo data is needed.