scholarly journals Will chronic e-cigarette use cause lung disease?

2015 ◽  
Vol 309 (12) ◽  
pp. L1398-L1409 ◽  
Author(s):  
Temperance R. Rowell ◽  
Robert Tarran
Keyword(s):  
Tobacco Smoking ◽  
Chronic Obstructive ◽  
Lung Cells ◽  
Cigarette Use ◽  
Obstructive Pulmonary Disease ◽  
Isolated Lung ◽  
Mammalian Lung ◽  
Never Smokers ◽  
New Generation

Chronic tobacco smoking is a major cause of preventable morbidity and mortality worldwide. In the lung, tobacco smoking increases the risk of lung cancer, and also causes chronic obstructive pulmonary disease (COPD), which encompasses both emphysema and chronic bronchitis. E-cigarettes (E-Cigs), or electronic nicotine delivery systems, were developed over a decade ago and are designed to deliver nicotine without combusting tobacco. Although tobacco smoking has declined since the 1950s, E-Cig usage has increased, attracting both former tobacco smokers and never smokers. E-Cig liquids (e-liquids) contain nicotine in a glycerol/propylene glycol vehicle with flavorings, which are vaporized and inhaled. To date, neither E-Cig devices, nor e-liquids, are regulated by the Food and Drug Administration (FDA). The FDA has proposed a deeming rule, which aims to initiate legislation to regulate E-Cigs, but the timeline to take effect is uncertain. Proponents of E-Cigs say that they are safe and should not be regulated. Opposition is varied, with some opponents proposing that E-Cig usage will introduce a new generation to nicotine addiction, reversing the decline seen with tobacco smoking, or that E-Cigs generally may not be safe and will trigger diseases like tobacco. In this review, we shall discuss what is known about the effects of E-Cigs on the mammalian lung and isolated lung cells in vitro. We hope that collating this data will help illustrate gaps in the knowledge of this burgeoning field, directing researchers toward answering whether or not E-Cigs are capable of causing disease.

scholarly journals WNT5a-ROR Signaling Is Essential for Alveologenesis

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 384 ◽  
Author(s):  
Changgong Li ◽  
Susan M Smith ◽  
Neil Peinado ◽  
Feng Gao ◽  
Wei Li ◽  
...  
Keyword(s):  
Lung Development ◽  
Lung Fibroblasts ◽  
Chronic Obstructive ◽  
Type I ◽  
Loss Of Function ◽  
Obstructive Pulmonary Disease ◽  
Alveolar Epithelial ◽  
Isolated Lung ◽  
And Migration

WNT5a is a mainly “non-canonical” WNT ligand whose dysregulation is observed in lung diseases such as idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD) and asthma. Germline deletion of Wnt5a disrupts embryonic lung development. However, the temporal-specific function of WNT5a remains unknown. In this study, we generated a conditional loss-of-function mouse model (Wnt5aCAG) and examined the specific role of Wnt5a during the saccular and alveolar phases of lung development. The lack of Wnt5a in the saccular phase blocked distal airway expansion and attenuated differentiation of endothelial and alveolar epithelial type I (AT1) cells and myofibroblasts. Postnatal Wnt5a inactivation disrupted alveologenesis, producing a phenotype resembling human bronchopulmonary dysplasia (BPD). Mutant lungs showed hypoalveolization, but endothelial and epithelial differentiation was unaffected. The major impact of Wnt5a inactivation on alveologenesis was on myofibroblast differentiation and migration, with reduced expression of key regulatory genes. These findings were validated in vitro using isolated lung fibroblasts. Conditional inactivation of the WNT5a receptors Ror1 and Ror2 in alveolar myofibroblasts recapitulated the Wnt5aCAG phenotype, demonstrating that myofibroblast defects are the major cause of arrested alveologenesis in Wnt5aCAG lungs. Finally, we show that WNT5a is reduced in human BPD lung samples, indicating the clinical relevance and potential role for WNT5a in pathogenesis of BPD.

scholarly journals Tobacco smoking and COVID-19: an old enemy in a new guise. Review of current publications

2020 ◽  
Vol 19 (3) ◽  
pp. 2604
Author(s):  
M. G. Gambaryan ◽  
O. M. Drapkina
Keyword(s):  
Tobacco Smoking ◽  
Poor Quality ◽  
Current Data ◽  
Adverse Outcomes ◽  
Quality Data ◽  
Chronic Obstructive ◽  
Cigarette Use ◽  
Obstructive Pulmonary Disease ◽  
Increased Risk ◽  
Novel Coronavirus

The review summarizes the current data on the relationship of tobacco smoking, e-cigarette use and the novel coronavirus infection COVID-19. The socio-demographic characteristics of patients with COVID-19 and associated diseases, which indicate a possible relationship between smoking and the disease, are analyzed. Recent large meta-analyzes demonstrating the increased risk of progression, the development of severe complications and adverse outcomes of COVID-19 in smokers, as well as in patients with chronic obstructive pulmonary disease, for which smoking is a leading risk factor, are shown. It is believed that tobacco smoking and e-cigarette use causes dose-dependent activation of the angiotensin-converting enzyme-2 receptor, by which virus penetrates to host cell. This may explain the higher risk of complicated COVID-19 in smokers and vapers. There is conflicting data because some studies showed some relatively low smoking prevalence among patients with COVID-19 compared with general population. This, in particular, was associated with poor-quality data collection about smoking, but, nevertheless, was the basis for hypotheses about the protective effect of nicotine against COVID-19. This issue needs further large independent studies, but it is clear so far that smoking is associated with the progression and adverse outcomes of COVID-19.

scholarly journals Hsp10 nuclear localization and changes in lung cells response to cigarette smoke suggest novel roles for this chaperonin

Open Biology ◽  
2014 ◽  
Vol 4 (10) ◽  
pp. 140125 ◽  
Author(s):  
Simona Corrao ◽  
Rita Anzalone ◽  
Melania Lo Iacono ◽  
Tiziana Corsello ◽  
Antonino Di Stefano ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Chronic Obstructive ◽  
Lung Cells ◽  
Obstructive Pulmonary Disease ◽  
Bronchial Epithelial ◽  
Pathological Conditions ◽  
Before And After ◽  
Nuclear Levels ◽  
Qualitative Changes

Heat-shock protein (Hsp)10 is the co-chaperone for Hsp60 inside mitochondria, but it also resides outside the organelle. Variations in its levels and intracellular distribution have been documented in pathological conditions, e.g. cancer and chronic obstructive pulmonary disease (COPD). Here, we show that Hsp10 in COPD undergoes changes at the molecular and subcellular levels in bronchial cells from human specimens and derived cell lines, intact or subjected to stress induced by cigarette smoke extract (CSE). Noteworthy findings are: (i) Hsp10 occurred in nuclei of epithelial and lamina propria cells of bronchial mucosa from non-smokers and smokers; (ii) human bronchial epithelial (16HBE) and lung fibroblast (HFL-1) cells, in vitro , showed Hsp10 in the nucleus, before and after CSE exposure; (iii) CSE stimulation did not increase the levels of Hsp10 but did elicit qualitative changes as indicated by molecular weight and isoelectric point shifts; and (iv) Hsp10 nuclear levels increased after CSE stimulation in HFL-1, indicating cytosol to nucleus migration, and although Hsp10 did not bind DNA, it bound a DNA-associated protein.

scholarly journals Exploring the gateway hypothesis of e-cigarettes and tobacco: a prospective replication study among adolescents in the Netherlands and Flanders

2021 ◽  
pp. tobaccocontrol-2021-056528
Author(s):  
Thomas Martinelli ◽  
Math J J M Candel ◽  
Hein de Vries ◽  
Reinskje Talhout ◽  
Vera Knapen ◽  
...  
Keyword(s):  
The Netherlands ◽  
Tobacco Use ◽  
Tobacco Smoking ◽  
Longitudinal Design ◽  
Positive Association ◽  
Cigarette Use ◽  
Convenience Sample ◽  
Frequent Use ◽  
Never Smokers

BackgroundStudies demonstrated that adolescent e-cigarette use is associated with subsequent tobacco smoking, commonly referred to as the gateway effect. However, most studies only investigated gateways from e-cigarettes to tobacco smoking. This study replicates a cornerstone study revealing a positive association between both adolescent e-cigarette use and subsequent tobacco use; and tobacco and subsequent e-cigarette use in the Netherlands and Flanders.DesignThe longitudinal design included baseline (n=2839) and 6-month (n=1276) and 12-month (n=1025) follow-up surveys among a school-based cohort (mean age: 13.62). Ten high schools were recruited as a convenience sample. The analyses involved (1) associations of baseline e-cigarette use and subsequent tobacco smoking among never smokers; (2) associations of e-cigarette use frequency at baseline and tobacco smoking frequency at follow-up; and (3) the association of baseline tobacco smoking and subsequent e-cigarette use among non-users of e-cigarettes.FindingsConsistent with prior findings, baseline e-cigarette use was associated with higher odds of tobacco smoking at 6-month (OR=1.89; 95% CI 1.05 to 3.37) and 12-month (OR=5.63; 95% CI 3.04 to 10.42) follow-ups. More frequent use of e-cigarettes at baseline was associated with more frequent smoking at follow-ups. Baseline tobacco smoking was associated with subsequent e-cigarette use (OR=3.10; 95% CI 1.58 to 6.06 at both follow-ups).ConclusionOur study replicated the positive relation between e-cigarette use and tobacco smoking in both directions for adolescents. This may mean that the gateway works in two directions, that e-cigarette and tobacco use share common risk factors, or that both mechanisms apply.

Association between E-cigarette use and chronic obstructive pulmonary disease in non-asthmatic adults in the USA

2020 ◽  
Author(s):  
Godfred O Antwi ◽  
Darson L Rhodes
Keyword(s):  
Sex Education ◽  
Smoking Status ◽  
Secondary Data ◽  
Chronic Obstructive ◽  
Behavioral Risk ◽  
Cigarette Use ◽  
Obstructive Pulmonary Disease ◽  
The Usa ◽  
Potential Link ◽  
Using Data

Abstract Background Concern about the health impacts of e-cigarette use is growing; however, limited research exists regarding potential long-term health effects of this behavior. This study explored the relationship between e-cigarette use and COPD in a sample of US adults. Methods A secondary data analysis using data from the 2018 Behavioral Risk Factor Surveillance Survey in the USA was computed to examine associations between e-cigarette use and COPD controlling for conventional cigarette smoking status, past month leisure physical activity and demographic characteristics including age, sex, education, race, marital status and body mass index. Results Significant associations between e-cigarette use and COPD among former combustible cigarette smokers and those who reported never using combustible cigarettes were found. Compared with never e-cigarette users, the odds of having COPD were significantly greater for daily e-cigarette users (OR = 1.53; 95% CI: 1.11–2.03), occasional users (OR = 1.43, 95% CI: 1.13–1.80) and former users (OR = 1.46 95% CI: 1.28–1.67). Conclusions Findings from this study indicate a potential link between e-cigarette use and COPD. Further research to explore the potential effects of e-cigarette on COPD is recommended.

scholarly journals ILC2 Cells Promote Th2 Cell Differentiation in AECOPD Through Activated Notch-GATA3 Signaling Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Min Jiang ◽  
Ren Cai ◽  
Jing Wang ◽  
Zheng Li ◽  
Dan Xu ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Peripheral Blood ◽  
Culture Supernatant ◽  
Th2 Cells ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Protein Levels ◽  
Th2 Cell

This study is to investigate the capacity of type 2 innate lymphoid cells (ILC2s) in regulating the Th2 type adaptive immune response of acute exacerbation of chronic obstructive pulmonary disease (AECOPD). The study enrolled healthy people, stable chronic obstructive pulmonary disease (COPD) patients, and AECOPD patients. Flow cytometry was used to detect Th2 and ILC2 cells in the peripheral blood. In addition, ILC2s from the peripheral blood of AECOPD patients were stimulated with PBS, IL-33, Jagged1, DAPT, IL-33+Jagged1, IL-33+DAPT, and IL-33+Jagged-1+DAP in vitro. The levels of cytokines in the culture supernatant were detected by ELISA and the culture supernatant was used to culture CD4 + T cells. The mRNA and protein levels of Notch1, hes1, GATA3, RORα, and NF-κB of ILC2s were detected by real-time PCR and Western blot. The proportion of Th2 and ILC2s was significantly increased in the peripheral blood of AECOPD patients, alone with the increased Notch1, hes1, and GATA3 mRNA levels. In vitro results showed that the mRNA and protein levels of Notch1, hes1, GATA3 and NF-κB were significantly increased after stimulation with Notch agonist, meanwhile, the level of type 2 cytokines were increased in the supernatant of cells stimulated with Notch agonist, and significantly promoted differentiation of Th2 cells in vitro. Disruption of Notch pathway weakened GATA3 expression and cytokine production, and ultimately affected the differentiation of Th2 cells. In conclusion, our results suggest that ILC2s can promote Th2 cell differentiation in AECOPD via activated Notch-GATA3 signal pathway.

scholarly journals Possible Implication of Hypoxia-mediated Incomplete Neutrophil Extracellular Trap Formation in Pneumonia-induced Exacerbation of Lung Diseases

2021 ◽  
Author(s):  
Sakiko Masuda ◽  
Kurumi Kato ◽  
Misato Ishibashi ◽  
Yuka Nishibata ◽  
Ayako Sugimoto ◽  
...  
Keyword(s):  
Lung Diseases ◽  
Actin Polymerization ◽  
Hypoxia Inducible Factor ◽  
Neutrophil Extracellular Trap ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Hypoxic Conditions ◽  
Pulmonary Arterial ◽  
Underlying Diseases

Abstract When patients with preexisting lung diseases, such as chronic obstructive pulmonary disease, interstitial pneumonitis, and pulmonary arterial hypertension, develop pneumonia, the complication often exacerbates the underlying diseases. Although neutrophil extracellular traps (NETs) are important components of innate immune system, the residue of NETs in the tissue can harm the host. We examined the expression of hypoxia-inducible factor 1α (HIF-1α) and NETs in the lungs of patients with lung diseases complicated with pneumonia, and investigated the properties of NETs generated under hypoxia. This study demonstrated that the amount of NETs in pulmonary lesions was greater in patients with pneumonia than in patients without pneumonia and displayed a positive correlation between the amount of NETs and HIF-1α expression. We further demonstrated that the formation of typical lytic NETs was suppressed and round-shaped NETs were generated under hypoxic conditions in vitro. These round NETs were resistant to digestion by the principal NET regulator, DNase I. Focusing on actin rearrangement in neutrophils stimulated under hypoxic conditions, we found that G-actin polymerization and F-actin degradation—both of which are observed time-dependently under normoxic conditions—were disrupted, suggesting that hypoxia mediated the incomplete NET formation. Moreover, neutrophils stimulated under hypoxic conditions possessed cytotoxicity. Accumulation of neutrophils that form degradation-resistant NETs and possess cytotoxicity, which are generated under hypoxic circumstances, are expected to be involved in exacerbation of underlying lung diseases complicated with pneumonia.

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