Acute Exposure to E‐Cigarette Vapor Causes Changes in Apoptotic Pathways in the Lung

Abstract

BackgroundElectronic cigarette usage is increasing at an alarming rate primarily because of reports implicating their use as safer than traditional cigarettes. However, little is known about the acute effects on lung injury and inflammation. These studies tested the hypothesis that acute exposure to e‐cigarette vapor would result in lung inflammation and injury.MethodsC57Bl/6 mice were exposed to e‐cigarette vapor consisting of 10 mg/mL nicotine in a 50/50 mixture of propylene glycol/vegetable glycerin (PG/VG) or PG/VG alone for 6 hr/day, 5 days/week for either 1 or 2 weeks. Lungs were excised and snap‐frozen for analysis. Lung homogenates were analyzed by western blot for pAKT, pSTAT3, PECAM, BCL‐2, and BAX. RNA was isolated for measurement of MMP9, KC, and VEGF by RT‐PCR.ResultspAKT protein expression was decreased (0.54 vs 1.0 relative density, p=0.02) and pSTAT3 was increased (1.7 vs 1.0 relative density, p=0.02) in the e‐cigarette exposed mice vs PG/VG exposed mice after 1 week of exposure. At 2 weeks, pSTAT3 remained increased (1.9 vs 1.0 relative density, p=0.01) and both BCL‐2 (2.5 vs 1.0 relative density, p=0.02) and BAX (1.7 vs 1.0 relative density, p<0.05) were increased in the exposed mice compared to mice exposed to PG/VG alone. No differences were observed in PECAM, MMP9, KC, or VEGF.ConclusionsAcute exposure to e‐cigarette vapor caused changes in signaling molecules associated with apoptosis. While we did not observe differences in the inflammatory pathways tested, additional inflammatory and apoptotic markers may yield insights into the acute effects of e‐cigarette vapor exposure on the lung.Support or Funding InformationNIH NHLBI R01 HL139348 02This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.