E-cigarette exposure with or without heating the e-liquid induces differential remodeling in the lungs and right heart of mice.

Introduction:
This text provides an analysis of a study examining the effects of electronic cigarette (EC) aerosol exposure with and without heating the e-liquid on the lungs and heart of mice. The study also investigates the roles of caspase recruitment domain-containing protein 9 (CaRD9) and NOD-like receptor family pyrin domain containing 3 (NLRP3) in EC exposure-induced cardiopulmonary injury.

Key Points:

* The study used a custom-built exposure system to expose C57BL/6 wild type (WT), CaRD9-/-, and NLRP3-/- mice to EC aerosol generated with or without heating the e-liquid for 3 h/day, 5 days/week for 6 months.
* Plasma cotinine levels were comparable in all groups, indicating similar nicotine absorption.
* EC exposure with heating (Ewh) significantly increased right ventricle (RV) free wall thickness at systole and diastole, but EC exposure without heating (Ewoh) caused a significant decrease in the wall thickness at systole.
* Ewh activated NF-κB and p38 MaPK inflammatory signaling in the lungs, but not in the RV, in a CaRD9- and NLRP3-dependent manner.
* Levels of circulatory inflammatory mediators were also elevated following Ewh, indicating systemic inflammation.
* Ewoh activated TGF-β1/SMaD2/3/α-SMa fibrosis signaling in the lungs but not the RV of WT mice.

Main Message:
The study demonstrates that EC aerosol exposure following Ewh or Ewoh induces differential cardiopulmonary remodeling and CaRD9 innate immune response and NLRP3 inflammasome contribute to the adverse effects. These findings suggest that EC aerosol exposure, whether heated or not, is detrimental to human health.

Getiye Y, Peterson MR, Phillips BD, Carrillo D, Bisha B, he G. E-cigarette exposure with or without heating the e-liquid induces differential remodeling in the lungs and right heart of mice. Journal of molecular and cellular cardiology. 2022;168:83-95. doi:10.1016/j.yjmcc.2022.04.014