Cigarette smoke exposure causes constriction of rat lung

Wright, J. L.; Sun, JP; Churg, Andrew

doi:10.1183/09031936.99.14510959

Cited by 19 publications

(11 citation statements)

References 27 publications

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“…1998; Wright et al. 1999); however, we have described that at lower concentrations, they do not provide a toxic effect to macrophages, but rather affects their function. Whilst E‐cigarettes are a relatively new product on the market, many papers now show that they too have toxic effects on a range of cells (Bahl et al.…”

Section: Discussionmentioning

confidence: 94%

Phagocytosis and Inflammation: Exploring the effects of the components of E-cigarette vapor on macrophages

et al. 2017

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E‐cigarettes are perceived as harmless; however, evidence of their safety is lacking. New data suggests E‐cigarettes discharge a range of compounds capable of physiological damage to users. We previously established that cigarette smoke caused defective alveolar macrophage phagocytosis. The present study compared the effect E‐cigarette of components; E‐liquid flavors, nicotine, vegetable glycerine, and propylene glycol on phagocytosis, proinflammatory cytokine secretion, and phagocytic recognition molecule expression using differentiated THP‐1 macrophages. Similar to CSE, phagocytosis of NTHi bacteria was significantly decreased by E‐liquid flavoring (11.65–15.75%) versus control (27.01%). Nicotine also decreased phagocytosis (15.26%). E‐liquid, nicotine, and E‐liquid+ nicotine reduced phagocytic recognition molecules; SR‐A1 and TLR‐2. IL‐8 secretion increased with flavor and nicotine, while TNF α, IL‐1β, IL‐6, MIP‐1α, MIP‐1β, and MCP‐1 decreased after exposure to most flavors and nicotine. PG, VG, or PG:VG mix also induced a decrease in MIP‐1α and MIP‐1β. We conclude that E‐cigarettes can cause macrophage phagocytic dysfunction, expression of phagocytic recognition receptors and cytokine secretion pathways. As such, E‐cigarettes should be treated with caution by users, especially those who are nonsmokers.

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Section: Discussionmentioning

confidence: 94%

Phagocytosis and Inflammation: Exploring the effects of the components of E-cigarette vapor on macrophages

et al. 2017

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“…Indeed, it has been demonstrated that direct administration of CS to lung explants produces constriction of the small airways. 31 This effect was related to endothelin in animals without previous CS exposure, and to the balance of oxidants and antioxidants in animals which have undergone smoke exposure in vivo. 31 To further assess the mechanism underlying the increase of airway resistance following short-term nose-only CS exposure, we have measured the ROS and lipid peroxidation in lungs.…”

Section: Discussionmentioning

confidence: 98%

“…31 This effect was related to endothelin in animals without previous CS exposure, and to the balance of oxidants and antioxidants in animals which have undergone smoke exposure in vivo. 31 To further assess the mechanism underlying the increase of airway resistance following short-term nose-only CS exposure, we have measured the ROS and lipid peroxidation in lungs. Oxidative stress results from an imbalance between radical-generating and radical-scavenging systems leading to cell membrane impairment or DNA damage.…”

Section: Discussionmentioning

confidence: 98%

Evaluation of the pulmonary effects of short-term nose-only cigarette smoke exposure in mice

Raza

Subramaniyan

John

et al. 2012

Exp Biol Med (Maywood)

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Much is known about the chronic effects of cigarette smoke (CS) on lung function and inflammation and development of chronic obstructive pulmonary disease. However, the underlying pathophysiological mechanisms related to the short-term exposure to CS are not fully understood. Here, we assessed the effect of CS generated by nine consecutive cigarettes per day for four days in a nose-only exposure system on airway resistance measured using forced oscillation technique, lung inflammation and oxidative stress in BALB/c mice. Control mice were exposed to air. Mice exposed to CS showed a significant increase of neutrophils and lymphocytes numbers in bronchoalveolar lavage (BAL). The total protein and endothelin levels in BAL fluid were significantly augmented suggesting an increase of alveolar-capillary barrier permeability. Similarly, airway resistance was significantly increased in the CS group compared with controls. Furthermore, reactive oxygen species and lipid peroxidation levels in lung tissue were significantly increased. The antioxidant activities of reduced glutathione, glutathione S transferase and superoxide dismutase were all significantly increased following CS exposure, indicating that CS could trigger adaptive responses that counterbalance the potentially damaging activity of oxygen radicals induced by CS exposure. In conclusion, our data indicate that short-term nose-only exposure to CS causes lung inflammation and increase of airway resistance mediated at least partly through the oxidative stress.

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“…Particles, nitrogen dioxide, and ozone are all oxidants that can trigger intracellular oxidative stress through the generation of free radicals (39)(40)(41). PM 2.5 likely shares mechanistic pathways with cigarette smoke exposure, which induces small airways constriction by stimulating endothelin release and via direct oxidant effects (42). O 3 exposure has been found to prime innate immunity and up-regulate expression of injury repair genes in mouse lung (43).…”

Section: Discussionmentioning

confidence: 99%

Short-Term Exposure to Air Pollution and Lung Function in the Framingham Heart Study

Rice

Ljungman²,

Wilker³

et al. 2013

Am J Respir Crit Care Med

173

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Rationale: Short-term exposure to ambient air pollution has been associated with lower lung function. Few studies have examined whether these associations are detectable at relatively low levels of pollution within current U.S. Environmental Protection Agency (EPA) standards. Objectives: To examine exposure to ambient air pollutants within EPA standards and lung function in a large cohort study. Methods: We included 3,262 participants of the Framingham Offspring and Third Generation cohorts living within 40 km of the Harvard Supersite monitor in Boston, Massachusetts (5,358 examinations, 1995Massachusetts (5,358 examinations, -2011) who were not current smokers, with previousday pollutant levels in compliance with EPA standards. We compared lung function (FEV 1 and FVC) after previous-day exposure to particulate matter less than 2.5 mm in diameter (PM 2.5 ), nitrogen dioxide (NO 2 ), and ozone (O 3 ) in the "moderate" range of the EPA Air Quality Index to exposure in the "good" range. We also examined linear relationships between moving averages of pollutant concentrations 1, 2, 3, 5, and 7 days before spirometry and lung function. Measurements and Main Results: Exposure to pollutant concentrations in the "moderate" range of the EPA Air Quality Index was associated with a 20.1-ml lower FEV 1 for PM 2.5 (95% confidence interval [CI], 233.4, 26.9), a 30.6-ml lower FEV 1 for NO 2 (95% CI, 260.9, 20.2), and a 55.7-ml lower FEV 1 for O 3 (95% CI, 2100.7, 210.8) compared with the "good" range. The 1-and 2-day moving averages of PM 2.5 , NO 2 , and O 3 before testing were negatively associated with FEV 1 and FVC.Conclusions: Short-term exposure to PM 2.5 , NO 2 , and O 3 within current EPA standards was associated with lower lung function in this cohort of adults.Keywords: chronic obstructive pulmonary disease; asthma; air pollutants; U.S. Environmental Protection Agency A substantial body of evidence has shown that modest shortterm increases in ambient air pollution, especially PM 2.5 (particles with an aerodynamic diameter < 2.5 mm) and ground level ozone (O 3 ), but also nitrogen dioxide (NO 2 ), increase risk of hospitalization for chronic obstructive pulmonary disease (COPD) and respiratory mortality (1-4). Several studies have found that short-term (1-3 d) increases in PM 2.5 , NO 2 , and O 3 are associated with decreases in FEV 1 , FVC, and/or peak expiratory flow rate in healthy subjects (5-11) and in those with preexisting COPD or asthma (12)(13)(14)(15).Air quality has improved substantially since the 1980s and 1990s, when many epidemiologic investigations of lung function and air pollution were completed (16). To protect public health and in accordance with its mandate, the EPA has continued to review the latest evidence and reevaluate air quality standards. Recently, the EPA lowered the annual standard for PM 2.5 from 15 to 12 mg/m 3 and reduced the daily Air Quality Index (AQI) cut-off for "moderate" PM 2.5 from 15.4 to 12 mg/m 3 . It remains unclear whether acute effects of criteria air pollutants (inclu...

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Cigarette smoke exposure causes constriction of rat lung

Cited by 19 publications

References 27 publications

Phagocytosis and Inflammation: Exploring the effects of the components of E-cigarette vapor on macrophages

Phagocytosis and Inflammation: Exploring the effects of the components of E-cigarette vapor on macrophages

Evaluation of the pulmonary effects of short-term nose-only cigarette smoke exposure in mice

Short-Term Exposure to Air Pollution and Lung Function in the Framingham Heart Study

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