AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY 审稿状态变化-刊鹿论文编译

Vaping Away Epithelial Integrity

Abstract:

Lung epithelial cells are the first line of defense against pathogens, chemicals, and xenobiotics. With each breath, we inhale a plethora of foreign antigens that may elicit a host immune response depending on the type of antigen or immunogen exposure, genetic predisposition, and structural integrity of lung epithelial cells. The asserted response also depends on the dose and chronicity of the exposure. The cellular complexity of the airways and alveoli is astounding and includes z50 different cell types, z12 of which are epithelial (1). Almost half of these epithelial cells are ciliated (pseudostratified columnar and cuboidal), with the remainder being comprised of goblet cells, basal cells, club cells, and, at the terminal alveolus, type I and type II alveolar epithelial cells (2). Together, these cells play a large and complex role in the host immune responses to constant bombardment from foreign insults (inhaled or aspirated). Epithelial injury initiates a variety of lung diseases, which may occur due to multiple factors. Cigarette smoke is a major risk factor, particularly in chronic obstructive pulmonary disease, asthma, and idiopathic pulmonary fibrosis. It is the principal preventable cause of death and disease in the United States (3) and possibly worldwide. With the growth in the use of e-cigarettes, also known as vaping, a current perception is that these tobacco alternatives are safer than cigarettes. This concept has rapidly led to an explosion in usage, especially among teens, who are attracted by the appealing flavors and ease of use. However, the field lacks understanding of the mechanisms related to the deleterious effects of e-cigarette vapor. In this issue of the Journal, Lin and colleagues (pp. 162–173) report on an investigation of the effects of e-cigarette vapor on CFTR (cystic fibrosis transmembrane conductance regulator) in airway epithelial cells, and they describe a previously unknown dose-dependent inhibitory effect of e-cigarette vapor on chloride anion transport by CFTR (4). Cigarette smoke induces defects in CFTR function (5), but the effects of e-cigarettes were unknown. Acquired dysfunction in CFTR resulting in impaired mucociliary transport and clearance has previously been noted in patients with chronic obstructive pulmonary disease, and especially in patients with chronic bronchitis (6, 7). Lin and colleagues establish that the pyrolysis product of e-cigarettes, acrolein, reduces the short-circuit chloride current without affecting cell survival. Toxic effects of e-cigarettes on airway epithelial cells, including a reduction in their viability, were previously reported (8), although the mechanisms remain elusive. The authors also found that, unlike cigarette smoke, e-cigarette vapor reduces ion conductance. The precise cause of this exclusive effect is not understood, but vaporization appears to trigger the dysfunction. Lin and colleagues also showed that primary human bronchial epithelial cells from donors were more sensitive to e-cigarette vapor-induced inhibition of CFTR-dependent chloride transport than Calu-3 cells, perhaps due to lower baseline expression of CFTR in human bronchial epithelial cells. This finding is important as we consider different cell types and cell lines to study different diseases. The authors detected a reduction in epithelial sodium channel activity, which, in contrast to CFTR dysfunction, is reported with cigarette smoke as well. Because CFTR also transports bicarbonate anions in addition to chloride anions, the e-cigarette vapor-induced CFTR dysfunction might increase the pH on the apical surface of airway epithelial cells and thus affect their physiology. The authors ruled out any changes in the pH by checking the pH in basolateral media of cells exposed to e-cigarette vapor. With longer exposure (60 min), they observed a reduction in transepithelial electrical resistance with e-cigarette vapor, suggesting compromised barrier integrity. Nonetheless, the precise mechanism and probable junctional proteins involved remain to be investigated (Figure 1). Because nicotine induces airway epithelial dysfunction by regulating CFTR function through nicotinic acetylcholine receptors (9), it likely has similar effects when inhaled as e-cigarette vapor. Like acrolein, nicotine has been associated with the formation of DNA adducts (10). Apart from DNA damage, it also reduces XPC and 8-oxoguanine DNA glycosylase 1/2 proteins, which are responsible for normal repair (11). The authors alluded to potential effects of nicotine on CFTR, but focused only on acrolein in this study. Likewise, other reactive aldehydes, reactive oxygen species (12), and heavy metals were not investigated in this study, although these agents may have a role in CFTR dysfunction in the airway epithelium (13). Acrolein has been shown to directly modify CFTR and inhibit channel gating (5). Considering that nicotine and acrolein form DNA adducts, it is plausible that they may directly or indirectly affect a variety of ion channels (Figure 1). Previous studies have shown that e-cigarettes dampen the ability of airway epithelial cells to respond to viral infections, increase inflammation, and enhance pneumococcal adherence (14–16). However, the precise mechanisms are not well understood. E-cigarette products, with or without nicotine, have been shown to inhibit expression of SPLUNC1 (short palate, lung, and nasal epithelial clone 1), a molecule required for host defense against human rhinovirus (15). These studies support the findings of Lin and colleagues, and suggest that e-cigarettes may have far-reaching effects in addition to those of nicotine or acrolein alone. Furthermore, other components present in e-cigarette vapor need to be tested for their effect on airway epithelium. Broadly, the current study by Lin and colleagues focuses attention on the involvement of ion channels in loss of epithelial function and how this may

Author Listing： Rohit Gaurav

Volume： 61

Pages： 127 - 129

DOI： 10.1165/rcmb.2019-0016ED

Language： English

Journal： American Journal of Respiratory Cell and Molecular Biology

AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY

AM J RESP CELL MOL

影响因子：5.9

是否综述期刊：否

是否OA：否

是否预警：不在预警名单内

发行时间：1989

ISSN：1044-1549

发刊频率：Monthly

收录数据库：SCIE/Scopus收录

出版国家/地区：UNITED STATES

出版社：American Thoracic Society

期刊介绍

The American Journal of Respiratory Cell and Molecular Biology publishes papers that report significant and original observations in the area of pulmonary biology. The focus of the Journal includes, but is not limited to, cellular, biochemical, molecular, developmental, genetic, and immunologic studies of lung cells and molecules.

《美国呼吸细胞和分子生物学杂志》发表的论文报告了肺生物学领域的重要和原始观察结果。该杂志的重点包括但不限于肺细胞和分子的细胞学、生物化学、分子学、发育学、遗传学和免疫学研究。

年发文量	96
国人发稿量	17
国人发文占比	17.71%
自引率	5.1%
平均录取率	较难
平均审稿周期	一般,3-8周
版面费	-
偏重研究方向	生物-呼吸系统
期刊官网	https://www.atsjournals.org/journal/ajrcmb
投稿链接	https://mc.manuscriptcentral.com/ajrcmb

质量指标占比

研究类文章占比	OA被引用占比	撤稿占比	出版后修正文章占比
96.88%	12.42%	0.00%	3.13%

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时间	预警情况
2024年02月发布的2024版	不在预警名单中
2023年01月发布的2023版	不在预警名单中
2021年12月发布的2021版	不在预警名单中
2020年12月发布的2020版	不在预警名单中

JCR分区 WOS分区等级：Q1区

版本	按学科	分区
WOS期刊SCI分区 WOS期刊SCI分区是指SCI官方（Web of Science）为每个学科内的期刊按照IF数值排序，将期刊按照四等分的方法划分的Q1-Q4等级，Q1代表质量最高，即常说的1区期刊。（2021-2022年最新版）
	CELL BIOLOGY	Q1
	RESPIRATORY SYSTEM	Q1
	BIOCHEMISTRY & MOLECULAR BIOLOGY	Q1

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分区表升级版（试行）旨在解决期刊学科体系划分与学科发展以及融合趋势的不相容问题。由于学科交叉在当代科研活动的趋势愈发显著，学科体系构建容易引发争议。为了打破学科体系给期刊评价带来的桎梏，“升级版方案”首先构建了论文层级的主题体系，然后分别计算每篇论文在所属主题的影响力，最后汇总各期刊每篇论文分值，得到“期刊超越指数”，作为分区依据。

分区表升级版（试行）的优势：一是论文层级的主题体系既能体现学科交叉特点，又可以精准揭示期刊载文的多学科性；二是采用“期刊超越指数”替代影响因子指标，解决了影响因子数学性质缺陷对评价结果的干扰。整体而言，分区表升级版（试行）突破了期刊评价中学科体系构建、评价指标选择等瓶颈问题，能够更为全面地揭示学术期刊的影响力，为科研评价“去四唯”提供解决思路。相关研究成果经过国际同行的认可，已经发表在科学计量学领域国际重要期刊。

《2019年中国科学院文献情报中心期刊分区表升级版（试行）》首次将社会科学引文数据库（SSCI）期刊纳入到分区评估中。升级版分区表（试行）设置了包括自然科学和社会科学在内的18个大类学科。基础版和升级版（试行）将过渡共存三年时间，推测在此期间各大高校和科研院所仍可能会以基础版为考核参考标准。提示：中科院分区官方微信公众号“fenqubiao”仅提供基础版数据查询，暂无升级版数据，请注意区分。

中科院分区查看说明

版本	大类学科	小类学科	Top期刊	综述期刊
	医学 1区	CELL BIOLOGY 细胞生物学 2区 RESPIRATORY SYSTEM 呼吸系统 2区 BIOCHEMISTRY & MOLECULAR BIOLOGY 生化与分子生物学 2区	否	是
2021年12月基础版	医学 2区	CELL BIOLOGY 细胞生物学 3区 RESPIRATORY SYSTEM 呼吸系统 2区 BIOCHEMISTRY & MOLECULAR BIOLOGY 生化与分子生物学 2区	否	否
2021年12月升级版	医学 1区	CELL BIOLOGY 细胞生物学 2区 RESPIRATORY SYSTEM 呼吸系统 2区 BIOCHEMISTRY & MOLECULAR BIOLOGY 生化与分子生物学 2区	否	是
2020年12月旧的升级版	医学 1区	CELL BIOLOGY 细胞生物学 2区 RESPIRATORY SYSTEM 呼吸系统 2区 BIOCHEMISTRY & MOLECULAR BIOLOGY 生化与分子生物学 2区	否	是
2022年12月最新升级版	医学 2区	CELL BIOLOGY 细胞生物学 2区 RESPIRATORY SYSTEM 呼吸系统 2区 BIOCHEMISTRY & MOLECULAR BIOLOGY 生化与分子生物学 2区	否	否