scholarly journals A comparative analysis of cannabis and tobacco smoke exposure on human airway epithelial cell gene expression, immune phenotype, and response to formoterol and budesonide treatment

2019 ◽  
Author(s):  
Jennifer A. Aguiar ◽  
Ryan D. Huff ◽  
Wayne Tse ◽  
Martin R. Stampfli ◽  
Brendan J. McConkey ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Epithelial Cell ◽  
Cell Viability ◽  
Tobacco Smoke ◽  
Barrier Function ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure ◽  
Airway Epithelial ◽  
And Oxidative Stress

AbstractGlobal recreational cannabis use is a potentially important public health issue that would benefit from experimental evidence to inform policy, regulations, and individual user practices. Comparative analyses between cannabis and tobacco smoke, the latter long reported to have negative impacts on respiratory health, may help provide context and provide clinically relevant evidence.To address this unmet need we performed a comparative study between cannabis and tobacco smoke exposure in the Calu-3 human airway epithelial cells using concentration-response and pharmacological intervention study designs with outcome measurements of cell viability, epithelial cell barrier function, cytokine profile, and transcriptomics.Our results demonstrate that cannabis smoke exposure reduces epithelial cell barrier function without impacting cell viability, accompanied by a cytokine profile associated with inflammation (elevated IL-6 and IL-8), barrier repair (elevated TGF-α and PDGF-AA) and suppressed antiviral immunity (decreased IP-10 and RANTES). Transcriptomic analyses revealed a cannabis smoke induced signature associated with suppressed antiviral genes and induction of oncogenic and oxidative stress pathways. Similar trends were observed for tobacco smoke exposure. A formoterol/budesonide intervention was unable to prevent cannabis smoke-induced reductions in antiviral pathways or normalize induction of oncogenic and oxidative stress responses.Our results show striking similarities between cannabis and tobacco smoke exposure on impairing barrier function, suppressing antiviral pathways, potentiating of pro-inflammatory mediators, and inducing oncogenic and oxidative stress gene expression signatures. Furthermore, we demonstrate that an intervention with formoterol and budesonide is unable to completely normalized cannabisinduced responses. Collectively our data suggest that cannabis smoke exposure is not innocuous and may possess many of the deleterious properties of tobacco smoke, warranting additional studies to support public policy, government regulations, and individual user practices.

Molecular Basis of Tobacco-Induced Bacterial Biofilms

2012 ◽  
Vol 147 (5) ◽  
pp. 876-884 ◽  
Author(s):  
Marcelo B. Antunes ◽  
John J. Chi ◽  
Zhi Liu ◽  
Natalia Goldstein-Daruech ◽  
James N. Palmer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Tobacco Smoke ◽  
Biofilm Formation ◽  
Smoke Exposure ◽  
Bacterial Biofilm ◽  
Tobacco Smoke Exposure ◽  
University Of Pennsylvania ◽  
Biofilm Growth

Objective To evaluate changes in the expression of biofilm-related genes when exposed to tobacco smoke and oxidative stress. Study Design Experimental, in vitro. Setting Laboratories of Rhinology and Microbiology, University of Pennsylvania. Subjects and Methods Bacterial biofilm mass was measured using crystal violet staining and measurement of the optical density. Biofilm-related genes of the Pseudomonas aeruginosa PAO1 strain ( pilF, flgK, lasI, lasB, rhlA, and algC) were studied following repetitive exposure to exogenous tobacco smoke and hydrogen peroxide. This was done using a reporter plasmid. Results After 1 exposure to smoke, there was no change in biofilm formation. However, after 2 and 3 exposures, the biofilm formed had an increased mass ( P < .05). With respect to oxidative stress in the form of H2O2, bacterial cultures demonstrated a dose- and time-dependent induction of biofilm formation compared with control conditions. Gene expression following repetitive smoke exposure demonstrated an increase in expression of pilF, flgK, algC, and lasI genes ( P < .05); a decrease in rhlA ( P < .05); and no significant change in the lasB gene ( P = 0.1). Gene expression following H2O2 exposure demonstrated an increase in pilF ( P < .05), whereas the other genes failed to demonstrate a statistical change. Conclusions Repetitive tobacco smoke exposure leads to molecular changes in biofilm-related genes, and exposure to oxidative stress in the form of H2O2 induces biofilm growth in PAO1. This could represent adaptative changes due to oxidative stress or chemically mediated through any of the several chemicals encountered in tobacco smoke and may explain increased biofilm formation in microbes isolated from smokers.

scholarly journals The Role of Green Tea and Oxidative Stress in Heart Remodeling Induced by Tobacco Smoke Exposure

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Elenize Jamas Pereira ◽  
Marcos Minicucci ◽  
Bertha Polegato ◽  
Priscila Portugal ◽  
Diego Batista ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Green Tea ◽  
Tobacco Smoke ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure ◽  
Heart Remodeling ◽  
And Oxidative Stress

Influence of prenatal waterpipe tobacco smoke exposure on reproductive hormones and oxidative stress of adult male offspring rats

Andrologia ◽  
2019 ◽  
Vol 51 (8) ◽  
Author(s):  
Nour A. Al‐Sawalha ◽  
Yehya M. Almahmmod ◽  
Karem H. Alzoubi ◽  
Omar F. Khabour ◽  
Weam N. Alyacoub
Keyword(s):  
Oxidative Stress ◽  
Adult Male ◽  
Tobacco Smoke ◽  
Reproductive Hormones ◽  
Smoke Exposure ◽  
Male Offspring ◽  
Tobacco Smoke Exposure ◽  
And Oxidative Stress

scholarly journals Reversible and permanent effects of tobacco smoke exposure on airway epithelial gene expression

2007 ◽  
Vol 8 (9) ◽  
pp. R201 ◽  
Author(s):  
Jennifer Beane ◽  
Paola Sebastiani ◽  
Gang Liu ◽  
Jerome S Brody ◽  
Marc E Lenburg ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tobacco Smoke ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure ◽  
Airway Epithelial

Comparison of Oxidative Effects of Electronic Cigarette and Tobacco Smoke Exposure Performed Experimentally

2021 ◽  
pp. 1-7
Author(s):  
Oktay Aslaner
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Smoke Exposure ◽  
Electronic Cigarette ◽  
Tobacco Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Exposure Group ◽  
Oxidative Effects

<b><i>Objective:</i></b> Cigarette smoking is a life-threatening habit that has rapidly spread in every socioeconomic part of the public worldwide. There exist mechanisms of nicotine delivery available to use in the hope of halting cigarette smoking, and the electronic cigarette (EC) is one of the common methods used for tobacco smoking replacement. This study aimed to investigate experimentally the oxidative effects of tobacco smoke and EC smoke which contain nicotine. <b><i>Method:</i></b> We constructed smoke circuit rooms for exposing the rats to EC or tobacco smoke. Three groups were created, the control group (<i>N</i> = 8); the electronic cigarette group (<i>N</i> = 8), exposure to electronic cigarette smoke for 2 h per day; and the tobacco group (<i>N</i> = 8), exposure to traditional cigarette smoke for 2 h per day. After the first and second week of exposure, blood samples were obtained, and serum oxidative stress index (OSI), paraoxonase 1 (PON1) activity, and prolidase levels were evaluated. <b><i>Results:</i></b> Higher values of OSI and prolidase levels were detected in the first week of EC or tobacco smoke exposure in both study groups (<i>p</i> &#x3c; 0.001) when compared with the control group, and partial decrements were observed in the second week. By contrast, elevated PON1 levels were observed in the second week after EC or tobacco smoke exposure. The highest OSI levels were observed in the tobacco smoke group (<i>p</i> &#x3c; 0.001). The lowest values of PON1 levels were detected in the first week of the electronic cigarette smoke group, and this decremental value was statistically different than normal, the second week of the electronic cigarette smoke group, the first week of the traditional cigarette smoke exposure group, and the second week of the traditional cigarette smoke exposure group values (<i>p</i> &#x3c; 0.000). <b><i>Conclusion:</i></b> Our results indicate that EC smoke induced oxidative stress. Therefore, ECs are potentially risky for human health and can lead to important health problems.

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