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Differential Effects of Propylene Glycol and Vegetable Glycerin on Epithelial Cells from the Upper and Lower Airways
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A3560 - Differential Effects of Propylene Glycol and Vegetable Glycerin on Epithelial Cells from the Upper and Lower Airways
Author Block: Y. Escobar, L. E. Brighton, P. W. Clapp, I. Jaspers; University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.
Background:
The use of electronic cigarettes (e-cigs) has been increasingly popular with one of the main questions being, are e-cigs ‘safer’ than traditional cigarettes? While the vapor generated by e-cigs contains lower amounts of known carcinogens as compared to traditional cigarettes, in vivo mouse studies and ex vivo human studies have shown that e-cig use might cause changes in immune responses. However, whether the base components of e-cig liquids (e-liquids), propylene glycol (PG) and vegetable glycerin (VG) cause changes in the airway mucosa indicative of modified immune responses is unknown.
Methods:
We generated condensates of PG, VG, and PG/VG vapor using a 3rd generation e-cig device set at 85W. Human nasal and bronchial epithelial cells (hNECs and hBECs) from healthy non-smokers were differentiated under the same conditions and treated for two hours with the different condensates. Basolateral supernatant, apical wash, and RNA were collected 2hrs and 24 hrs post exposure. Multi-plex ELISA was used to measure changes in 30 mediators. Data were normalized to respective vehicle controls and analyzed using one sample t-test.
Results:
Of the 30 cytokines measured in the basolateral supernatants, 22 cytokines were detectable. IL-7, VEGF, IL-12p40, TARC and IL-4 were differentially expressed in hNECs and hBECs. PG, VG, or PG/VG differentially affected levels of several cytokines in hNECS and hBECs. Eotaxin-3/CCL26, a chemoattractant for eosinophils and lymphocytes, was reduced in hNECs treated with PG condensate 2 hrs post-exposure. At 24 hrs post-exposure, PG, VG, and PG/VG-treated hNECs showed reduced eotaxin-3/CCL26 levels. This drop in eotaxin-3/CCL26 levels was not observed in hBECs treated with the different condensates at any time point. Levels of VEGF, a pro-angiogenic factor, was increased in PG-treated hNECs 24 hrs post-exposure which was not seen in hBECs. IL-8, a pro-inflammatory cytokine, was increased in hNECs treated with VG condensate 2 hrs post-exposure, and in hBECs 24 hrs post-exposure.
Conclusions:
Our data indicate that hNECs and hBECs differentiated under identical conditions secrete different cytokine profiles. In addition, there are differential effects of the e-liquid components PG, VG, and PG/VG on hNECs and hBECs, with hNECs appearing more responsive to these exposures. Our data contribute to the understanding of potential immune modifications of aerosolized PG and VG components of e-liquids.
Author Block: Y. Escobar, L. E. Brighton, P. W. Clapp, I. Jaspers; University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.
Background:
The use of electronic cigarettes (e-cigs) has been increasingly popular with one of the main questions being, are e-cigs ‘safer’ than traditional cigarettes? While the vapor generated by e-cigs contains lower amounts of known carcinogens as compared to traditional cigarettes, in vivo mouse studies and ex vivo human studies have shown that e-cig use might cause changes in immune responses. However, whether the base components of e-cig liquids (e-liquids), propylene glycol (PG) and vegetable glycerin (VG) cause changes in the airway mucosa indicative of modified immune responses is unknown.
Methods:
We generated condensates of PG, VG, and PG/VG vapor using a 3rd generation e-cig device set at 85W. Human nasal and bronchial epithelial cells (hNECs and hBECs) from healthy non-smokers were differentiated under the same conditions and treated for two hours with the different condensates. Basolateral supernatant, apical wash, and RNA were collected 2hrs and 24 hrs post exposure. Multi-plex ELISA was used to measure changes in 30 mediators. Data were normalized to respective vehicle controls and analyzed using one sample t-test.
Results:
Of the 30 cytokines measured in the basolateral supernatants, 22 cytokines were detectable. IL-7, VEGF, IL-12p40, TARC and IL-4 were differentially expressed in hNECs and hBECs. PG, VG, or PG/VG differentially affected levels of several cytokines in hNECS and hBECs. Eotaxin-3/CCL26, a chemoattractant for eosinophils and lymphocytes, was reduced in hNECs treated with PG condensate 2 hrs post-exposure. At 24 hrs post-exposure, PG, VG, and PG/VG-treated hNECs showed reduced eotaxin-3/CCL26 levels. This drop in eotaxin-3/CCL26 levels was not observed in hBECs treated with the different condensates at any time point. Levels of VEGF, a pro-angiogenic factor, was increased in PG-treated hNECs 24 hrs post-exposure which was not seen in hBECs. IL-8, a pro-inflammatory cytokine, was increased in hNECs treated with VG condensate 2 hrs post-exposure, and in hBECs 24 hrs post-exposure.
Conclusions:
Our data indicate that hNECs and hBECs differentiated under identical conditions secrete different cytokine profiles. In addition, there are differential effects of the e-liquid components PG, VG, and PG/VG on hNECs and hBECs, with hNECs appearing more responsive to these exposures. Our data contribute to the understanding of potential immune modifications of aerosolized PG and VG components of e-liquids.
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