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

Yoko Ito,Tadayuki Sato,Kana Oshinden,Koichiro Asano,Masayuki Tanaka,Keiko Yokoyama,Naokata Kutsuzawa,Sanae Isaki,Chinatsu Kohno,Shama Ahmad

doi:10.1371/journal.pone.0242789

Yoko Ito, Tadayuki Sato + Show 8 more

Open Access

https://doi.org/10.1371/journal.pone.0242789

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Journal: PloS one	Publication Date: Nov 25, 2020
Citations: 17	License type: CC BY 4.0

Affiliation: Tokai University

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.

Highlights

Cigarette smoking is well-known to cause disastrous respiratory diseases such as chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF) and lung cancer [1]
To explore which genes in alveolar epithelial (ATI)-like cells were modified by IQOS cigarette smoke extract (CSE), a microarray analysis was conducted with samples from cells stimulated by 10 or 20% IQOS CSE for 6 h
Two oxidative stress response genes, Glutathione S-Transferase Alpha 3 (Gsta3) and Heme Oxygenase-1 (Hmox-1), were identified among the top ten genes upregulated by 20% IQOS CSE at 6 h (Table 1)

Summary

Introduction

Cigarette smoking is well-known to cause disastrous respiratory diseases such as chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF) and lung cancer [1]. Newer forms of smoking devices, known as electric cigarettes (e-cigarettes) and heat-not burn (HNB) cigarettes, have increased in popularity in the past decade. E-cigarettes with nicotine are not publicly sold in Japan except for personal import, as they are regulated by the Medical Products and Medical Devices Act under the jurisdiction of the Ministry of Health, Labor and Welfare. In 2016 Japan became the first country in the world to sell I-QuitOrdinary-Smoking (IQOS), one of HNB cigarette products.

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