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 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.

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.

Secondhand tobacco smoke, arterial stiffness, and altered circadian blood pressure patterns are associated with lung inflammation and oxidative stress in rats

2012 ◽  
Vol 302 (3) ◽  
pp. H818-H825 ◽  
Author(s):  
Nicole J. Gentner ◽  
Lynn P. Weber
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Stiffness ◽  
Tobacco Smoke ◽  
Pulse Wave ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure ◽  
Secondhand Tobacco Smoke ◽  
Blood Pressure Patterns

Chronic smoking and secondhand tobacco smoke exposure are major risk factors for cardiovascular disease that are known to adversely alter the structural and mechanical properties of arteries. The objective of this study was to determine the effects of subchronic secondhand tobacco smoke exposure on circadian blood pressure patterns, arterial stiffness, and possible sources of oxidative stress in conscious, unsedated radiotelemetry-implanted rats. Pulse wave change in pressure over time (dP/d t) was used an indicator of arterial stiffness and was compared with both structural (wall thickness) and functional (nitric oxide production and bioactivity and endothelin-1 levels) features of the arterial wall. In addition, histology of lung, heart, and liver was examined as well as pulmonary and hepatic detoxifying enzyme activity (cytochrome P450, specifically CYP1A1). Subchronic secondhand tobacco smoke exposure altered the circadian pattern of heart rate and blood pressure, with a loss in the normal dipping pattern of blood pressure during sleep. Secondhand tobacco smoke exposure also increased pulse wave dP/d t in the absence of any structural modifications in the arterial wall. Furthermore, although nitric oxide production and endothelin-1 levels were not altered by secondhand tobacco smoke, there was increased inactivation of nitric oxide as indicated by peroxynitrite production. Increased lung neutrophils or pulmonary CYP1A1 may be responsible for the increase in oxidative stress in rats exposed to secondhand tobacco smoke. In turn, this may be related to the observed failure of blood pressure to dip during periods of sleep and a possible increase in arterial stiffness.

scholarly journals Ten Years and More of ‘Biosciences’ in CORESTA - A Brief Historic Overview

2013 ◽  
Vol 25 (5) ◽  
pp. 563-571
Author(s):  
W Röper
Keyword(s):  
Tobacco Smoke ◽  
Toxicity Testing ◽  
Study Groups ◽  
Smoking Behaviour ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure ◽  
Design Parameters ◽  
Smoke Toxicity ◽  
Clear Trend

AbstractIn June 2001, the CORESTA2 Board formally decided to broaden the scope of CORESTA by engaging in biosciences (other than tobacco agronomy and phytopathology), starting with in vitro toxicity testing and biomarkers of tobacco (smoke) exposure. Until then, work addressing biological aspects of smoking had only been done since 1996 by a special committee within CORESTA, reporting directly to the Scientific Commission, the Smoking Behaviour Committee. Membership of that committee was - similar to ACAC3 - by invitation only. The broadened scope consequently led to the re-shaping of the then Study Groups ‘Smoke’ and ‘Technology’ into ‘Smoke Science’ (SS) and ‘Product Technology’ (PT).Subsequently, three Sub-Groups (SG) and Task Forces (TF) were set up, reflecting this change: i) SG Smoking Behaviour (name change of former Committee in 2001), ii) TF ‘Nicotine Intake’ (2001, later on named ‘Nicotine Uptake’, disbanded in 2009) and iii) TF ‘In vitro Toxicity Testing of Tobacco Smoke’ (2002). Finally, a new SG ‘Biomarkers’ was launched in 2009 with a wider scope than its predecessor TF ‘Nicotine Uptake’. The work of these groups has had and still has significant impact on the scientific work within CORESTA, leading to numerous presentations at CORESTA meetings and publications in peer-reviewed journals.This paper provides a brief analysis of some 270 presentations and posters addressing tobacco smoke toxicity, human smoking behaviour or biomarkers, delivered at CORESTA Congresses and SSPT Joint Meetings between 1993 and 2011. More than 50% of these papers covered different aspects of toxicology, mainly in vitro toxicity testing methodologies, smoke exposure systems and other equipments. Other papers described the influence of cigarette design parameters on smoke toxicity. Approaches to human risk assessment were presented, including the search for suitable in vitro models of the major smoking related human diseases.CORESTA began discussing smoking behaviour topics at their Vienna meeting in 1995 and received five respective presentations there; indeed, the issue has various aspects, from smoking topography and human smoke yield to smoke uptake, deposition and retention, and… Why do people smoke at all?As early as 1996, a presentation was given on the determination of urinary mutagenicity in volunteers exposed to ETS (environmental tobacco smoke), apparently indicating a need for CORESTA to engage in this field and to face new challenges. Indeed, our knowledge of biomarkers and how to measure them has increased considerably over the years, and there is a clear trend towards using this knowledge for conducting clinical studies into the assessment of ‘modified risk tobacco products’.

scholarly journals The role of oxidative stress and lipid peroxidation in ventricular remodeling induced by tobacco smoke exposure after myocardial infarction

Clinics ◽  
2009 ◽  
Vol 64 (7) ◽  
Author(s):  
Daniella R. Duarte ◽  
Marcos F. Minicucci ◽  
Paula S. Azevedo ◽  
Beatriz B. Matsubara ◽  
Luiz S. Matsubara ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Lipid Peroxidation ◽  
Tobacco Smoke ◽  
Ventricular Remodeling ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure

Effect of waterpipe tobacco smoke exposure during lactation on learning and memory of offspring rats: Role of oxidative stress

Life Sciences ◽  
2019 ◽  
Vol 227 ◽  
pp. 58-63 ◽  
Author(s):  
Nour A. Al-Sawalha ◽  
Karem H. Alzoubi ◽  
Omar F. Khabour ◽  
Weam Alyacoub ◽  
Yehya Almahmood
Keyword(s):  
Oxidative Stress ◽  
Learning And Memory ◽  
Tobacco Smoke ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure

Effects of Cola-Flavored Beverages and Caffeine on Streptococcus mutans Biofilm Formation and Metabolic Activity

2017 ◽  
Vol 41 (4) ◽  
pp. 294-299 ◽  
Author(s):  
Roger P Dotsey ◽  
Elizabeth A S Moser ◽  
George J Eckert ◽  
Richard L Gregory
Keyword(s):  
Streptococcus Mutans ◽  
Metabolic Activity ◽  
Crystal Violet ◽  
Biofilm Formation ◽  
Bacterial Biofilm ◽  
Water Soluble ◽  
High Fructose Corn Syrup ◽  
Biofilm Growth ◽  
High Fructose

Objective: To examine the effects of cola-flavored beverages and caffeine on growth and metabolism of Streptococcus mutans biofilm. This study was designed to determine if carbonated beverages or caffeine can increase S. mutans growth and biofilm formation and metabolic activity in vitro, potentially leading to increased S. mutans-associated cariogenicity in children that consume them. Study Design: Six different cola-flavored products, plus pure caffeine, and pure high fructose corn syrup (HFCS), at different concentrations similar to those in the beverages were tested. A 16-hour culture of S. mutans was treated with different dilutions in bacteriological media. To test for the effect on biofilm formation, the biofilm was stained with crystal violet. The absorbance was determined to evaluate biofilm growth. Biofilm metabolic activity was measured based on biofilm having the ability to reduce XTT to a water-soluble orange compound. Results: The inclusion of HFCS in the beverages, as well as pure HFCS, significantly enhanced bacterial biofilm formation and metabolic activity. Pure caffeine and the presence of caffeine in beverages did not significantly increase biofilm formation, but pure caffeine significantly increased metabolism, and Diet Coke had significantly greater metabolic activity than Caffeine-Free Diet Coke. Conclusions: HFCS increases both the biofilm formation and metabolism of S. mutans, and caffeine in some cases increases metabolism of S. mutans.

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