Heat-Not-Burn cigarette induces oxidative stress response in primary rat alveolar epithelial cells

PLoS One. 2020 Nov 25;15(11):e0242789. doi: 10.1371/journal.pone.0242789. eCollection 2020.

Abstract

There has been an increase in the usage of heat-not-burn (HNB) cigarette products. However, their effects on alveolar epithelial cells (AECs) remain unknown. AECs are the target cells of conventional cigarette smoking-related respiratory diseases such as chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis and lung cancer whose pathogenesis involves oxidative stress. In this study, primary rat AECs were isolated, cultured and stimulated by HNB cigarette smoke extract (CSE). Our data indicate that rat AECs exposed to HNB CSE induced oxidative stress response genes (e.g. Hmox-1, Gsta1, Gsta3 and Nqo1). We also compared the oxidative stress response between two different types of AECs, alveolar type I-like (ATI-like) cells and type II (ATII) cells, and between two different types of cigarette, HNB cigarettes and conventional cigarettes. The expressions of Gsta1, Gsta3 and Nqo1 were higher in ATII cells than ATI-like cells in response to HNB and conventional cigarettes, but there was no significant difference in their expression levels between HNB cigarette and conventional cigarette. Taken together, our results suggest that HNB cigarettes have the similar potential as conventional cigarette products to induce oxidative stress response in AECs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alveolar Epithelial Cells / drug effects*
  • Alveolar Epithelial Cells / pathology
  • Animals
  • Cigarette Smoking / adverse effects*
  • Disease Models, Animal
  • Electronic Nicotine Delivery Systems
  • Hot Temperature / adverse effects
  • Humans
  • Nicotiana / adverse effects
  • Oxidation-Reduction / drug effects
  • Oxidative Stress / drug effects*
  • Primary Cell Culture
  • Pulmonary Alveoli / drug effects*
  • Pulmonary Alveoli / pathology
  • Pulmonary Disease, Chronic Obstructive / chemically induced
  • Rats
  • Smoke / adverse effects

Substances

  • Smoke

Grants and funding

The research work described in this manuscript has been supported by the Grant-in-Aid for Scientific Research from The Ministry of Education, Culture, Sports, Science and Technology (20K17229) and Tokai University School of Medicine that were awarded to Kana Oshinden, and grant from Japan Society of Tobacco Control awarded to Yoko Ito. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.