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E-Cigarette Synthetic Cooling Agent WS-23 and Nicotine Aerosols Differentially Modulate Airway Epithelial Cell Responses

Marko Manevski, Dinesh Devadoss, Shaiesh Yogeswaran, Irfan Rahman, View ORCID ProfileHitendra S. Chand
doi: https://doi.org/10.1101/2022.06.20.496868
Marko Manevski
1Department of Immunology and Nano-Medicine, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, USA
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Dinesh Devadoss
1Department of Immunology and Nano-Medicine, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, USA
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Shaiesh Yogeswaran
2Department of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA
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Irfan Rahman
2Department of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA
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Hitendra S. Chand
1Department of Immunology and Nano-Medicine, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, USA
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  • ORCID record for Hitendra S. Chand
  • For correspondence: hchand@fiu.edu
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Abstract

Electronic cigarette (e-cig) aerosol/vape exposures are strongly associated with pulmonary dysfunctions, and the airway epithelial cells (AECs) of respiratory passages play a pivotal role in understanding this association. However, not much is known about the effect of synthetic cooling agents such as WS-23 on AECs. WS-23 is a synthetic menthol-like cooling agent widely used to enhance the appeal of e-cigs and to suppress the harshness and bitterness of other e-cig constituents. Using primary human AECs, we compared the effects of aerosolized WS-23 with propylene glycol/vegetable glycerin (PG/VG) vehicle control and nicotine aerosol exposures. AECs treated with 3% WS-23 aerosols showed a significant increase in viable cell numbers compared to PG/VG-vehicle aerosol exposed cells and cell growth was comparable following 2.5% nicotine aerosol exposure. AEC inflammatory factors, IL-6 and ICAM-1 levels were significantly suppressed by WS-23 aerosols compared to PG/VG-controls. When differentiated AECs were challenged with WS-23 aerosols, there was a significant increase in MUC5AC+ goblet cells with no discernible change in SCGB1A1+ secretory cells. Compared to PG/VG-controls, WS-23 or nicotine aerosols presented with increased goblet cell numbers, but there was no synergistic effect of WS-23+nicotine combination exposure. Thus, WS-23 and nicotine aerosols modulate the AEC responses and induce goblet cell hyperplasia, which could impact the airway physiology and susceptibility to respiratory diseases.

Competing Interest Statement

The authors have declared no competing interest.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission.
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Posted June 21, 2022.
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E-Cigarette Synthetic Cooling Agent WS-23 and Nicotine Aerosols Differentially Modulate Airway Epithelial Cell Responses
Marko Manevski, Dinesh Devadoss, Shaiesh Yogeswaran, Irfan Rahman, Hitendra S. Chand
bioRxiv 2022.06.20.496868; doi: https://doi.org/10.1101/2022.06.20.496868
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E-Cigarette Synthetic Cooling Agent WS-23 and Nicotine Aerosols Differentially Modulate Airway Epithelial Cell Responses
Marko Manevski, Dinesh Devadoss, Shaiesh Yogeswaran, Irfan Rahman, Hitendra S. Chand
bioRxiv 2022.06.20.496868; doi: https://doi.org/10.1101/2022.06.20.496868

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