Maternal E-cigarette Vaping Enhances Development of Allergic Asthma In the Offspring

American Thoracic Society
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Conference Proceeding
American Journal of Respiratory and Critical Care Medicine, 2017
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Rationale: E-cigarettes (eCig) are being considered as an alternative to quit cigarette smoking (CS) while their long-term safety and effect on lung patho-physiology are not known. Maternal eCig-vaping may be considered as a safer CS-replacement during pregnancy. Thus the effect of maternal eCig vaping needs further assessment, particularly the effect this has on offspring and development of allergic asthma later in life. Combining mouse models of maternal vaping and allergic asthma and human airway smooth muscle cells (ASM) in vitro we tested whether maternal eCig vaping enhances features of allergic asthma in the offspring. Methods: Female BALB/c mice were vaped with either eCig vapour (± nicotine) or CS+eCig (+nicotine) or room air (control group). The eCig vaping was started prior to mating and continued during gestation and lactation while CS-exposure was used prior to mating and replaced with eCig during gestation and mating. The female offspring from these mothers were subjected to an ovalbumin (OVA)-induced allergic asthma model. 24 hours after the last aerosolized OVA or saline challenge, lung function measurements were performed using flexiVent (Scireq, Canada) to increasing concentration of methacholine (MCh). Airway inflammation was assessed by counting total immune cell influx in BAL fluid. Human ASM cells were treated with varying concentrations of eCig liquid condensate and key parameters of mitochondrial function were measured with a Seahorse XF analyzer. Results: Repeated allergen-exposure induced Th2-driven inflammation in OVA-exposed mice, characterized by massive influx of leukocytes predominantly eosinophils (OVA: 3x105±8.3x104 vs Saline: 1.1x102±1x102) and to some extent neutrophils (OVA: 1.3x104±4.4x103 vs Saline: 1.3x102±1.1x102) into the airways. The effect of allergen on airway eosinophilia was significantly enhanced in the offsprings from eCig OVA (+Nic)-exposed mothers when compared with eCig OVA (-Nic) or CS+eCig animals. OVA-exposed mice were found to be hyperresponsive (increased airway resistance) to inhaled MCh when compared to saline controls. Interestingly we found augmented airway resistance in the eCig-OVA(+Nic) group when compared to OVA or eCig OVA (-Nic) alone (p<0.05). While replacing CS with eCig [CS+eCig (+Nic)] was found to have the same effect on airway resistance as in eCig-OVA(+Nic) mice. Mechanistically, we found eCig (+Nic) at 24-hours dose-dependently reduced mitochondrial oxygen consumption rate using seahorse bioanalyzer which may partly explain enhanced features of allergic asthma in the offspring. Conclusions: Our study suggests that maternal eCig vaping enhanced and worsened features of allergic asthma and this could be attributed to aberrant mitochondrial function in the offspring.
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