Nicotine alters mucin rheological properties

Chen, Eric; Sun, Albert Y.; Chen, Chi-Shuo; Mintz, Alexander; Chin, Wei‐Chun

doi:10.1152/ajplung.00396.2012

Cited by 31 publications

(18 citation statements)

References 59 publications

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“…Nicotine hinders the hydration of mucus,28 promotes Ca 2+ influx in airway smooth muscle cells,29 blocks neutrophil apoptosis30 and induces pro-inflammatory dendritic cell responses 31. Smoke generated from high-dose nicotine cigarettes induces more emphysematous changes than low-dose nicotine cigarettes, in elastase-treated rats 32.…”

Section: Discussionmentioning

confidence: 99%

Chronic electronic cigarette exposure in mice induces features of COPD in a nicotine-dependent manner

García-Arcos

Geraghty

Baumlin

et al. 2016

Thorax

276

263

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BackgroundThe use of electronic (e)-cigarettes is increasing rapidly, but their lung health effects are not established. Clinical studies examining the potential long-term impact of e-cigarette use on lung health will take decades. To address this gap in knowledge, this study investigated the effects of exposure to aerosolised nicotine-free and nicotine-containing e-cigarette fluid on mouse lungs and normal human airway epithelial cells.MethodsMice were exposed to aerosolised phosphate-buffered saline, nicotine-free or nicotine-containing e-cigarette solution, 1-hour daily for 4 months. Normal human bronchial epithelial (NHBE) cells cultured at an air-liquid interface were exposed to e-cigarette vapours or nicotine solutions using a Vitrocell smoke exposure robot.ResultsInhalation of nicotine-containing e-cigarettes increased airway hyper-reactivity, distal airspace enlargement, mucin production, cytokine and protease expression. Exposure to nicotine-free e-cigarettes did not affect these lung parameters. NHBE cells exposed to nicotine-containing e-cigarette vapour showed impaired ciliary beat frequency, airway surface liquid volume, cystic fibrosis transmembrane regulator and ATP-stimulated K+ ion conductance and decreased expression of FOXJ1 and KCNMA1. Exposure of NHBE cells to nicotine for 5 days increased interleukin (IL)-6 and IL-8 secretion.ConclusionsExposure to inhaled nicotine-containing e-cigarette fluids triggered effects normally associated with the development of COPD including cytokine expression, airway hyper-reactivity and lung tissue destruction. These effects were nicotine-dependent both in the mouse lung and in human airway cells, suggesting that inhaled nicotine contributes to airway and lung disease in addition to its addictive properties. Thus, these findings highlight the potential dangers of nicotine inhalation during e-cigarette use.

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Section: Discussionmentioning

confidence: 99%

Chronic electronic cigarette exposure in mice induces features of COPD in a nicotine-dependent manner

García-Arcos

Geraghty

Baumlin

et al. 2016

Thorax

276

263

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“…27 Although not yet examined for gallbladder epithelium, in the airway nAChRs are expressed by epithelial cells 28,29 and nicotine has been demonstrated to decrease mucus transport, 30 increase mucin expression and mucus secretion, 31,32 alter mucus hydration, and increase the viscosity of mucus. 33 Nicotine also has been described to cause relaxation of guinea pig gallbladder by a mechanism independent of nAChRs. 34 Whether or not environmental exposure of dogs to nicotine could increase odds of GBM formation in dogs was not investigated in our study but should be considered.…”

Section: Discussionmentioning

confidence: 99%

Association of Gallbladder Mucocele Histologic Diagnosis with Selected Drug Use in Dogs: A Matched Case‐Control Study

Gookin

Correa

Peters

et al. 2015

Veterinary Internal Medicne

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BackgroundThe cause of gallbladder mucocele (GBM) formation in dogs currently is unknown. Many available drugs represent a newer generation of xenobiotics that may predispose dogs to GBM formation.ObjectiveTo determine if there is an association between the histologic diagnosis of GBM in dogs and administration of selected drugs.AnimalsEighty‐one dogs with a histologic diagnosis of GBM and 162 breed, age, and admission date‐matched control dogs from a single referral institution.MethodsMedical records of dogs with GBM and control dogs from 2001 to 2011 were reviewed. Owner verification of drug history was sought by a standard questionnaire. Reported use of heartworm, flea, and tick preventatives as well as nonsteroidal anti‐inflammatory drugs, analgesics, corticosteroids, or medications for treatment of osteoarthritis was recorded.ResultsDogs with GBM were 2.2 times as likely to have had reported use of thyroxine (as a proxy for the diagnosis of hypothyroidism) as control dogs (95% confidence interval [CI], 0.949–5.051), 3.6 times as likely to have had reported treatment for Cushing's disease (95% CI, 1.228–10.612), and 2.3 times as likely to have had reported use of products containing imidacloprid (95% CI, 1.094–4.723). Analysis of a data subset containing only Shetland sheepdogs (23 GBM and 46 control) indicated that Shetland sheepdogs with GBM formation were 9.3 times as likely to have had reported use of imidacloprid as were control Shetland sheepdogs (95% CI, 1.103–78.239).Conclusions and Clinical ImportanceThis study provides evidence for an association between selected drug use and GBM formation in dogs. A larger epidemiologic study of Shetland sheepdogs with GBM formation and exposure to imidacloprid is warranted.

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“…Specifically, in a rodent study by Mishra et al, nicotine inhibited allergen-induced inflammation, eosinophilia, leukotriene release, allergen-specific IgE levels, and Th2 cytokine levels without significantly altering airway mucosa morphology or airway resistance [57]. In contrast, nicotine has been reported to increase airway mucus viscosity [58] and enhance mucus production in human bronchial epithelial cells, which is dependent on the expression of alpha7-nAChR [59]. Nicotine-induced anti-inflammatory responses in the lung have also been associated with increased susceptibility to respiratory viral infections due to reduced migration of immune cells to sites of infection [60].…”

Section: E-liquid Components and Their Effects On The Lungmentioning

confidence: 99%

Electronic Cigarettes: Their Constituents and Potential Links to Asthma

Clapp

Jaspers

2017

Curr Allergy Asthma Rep

169

152

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Purpose of Review Vaping is gaining popularity in the USA, particularly among teens and young adults. While e-cigs are commonly represented as safer alternatives to tobacco cigarettes, little is known regarding the health effects of their short- or long-term use, especially in individuals with pre-existing respiratory diseases such as asthma. Flavored e-cig liquids (e-liquids) and e-cig aerosols contain airway irritants and toxicants that have been implicated in the pathogenesis and worsening of lung diseases. In this review, we will summarize existing data on potential health effects of components present in e-cig aerosols, such as propylene glycol, vegetable glycerin, nicotine, and flavorings, and discuss their relevance in the context of asthma. Recent Findings Recent survey data indicate that adolescents with asthma had a higher prevalence of current e-cig use (12.4%) compared to their non-asthmatics peers (10.2%) and conveyed positive beliefs about tobacco products, especially e-cigs. Similarly, a study conducted among high school students from Ontario, Canada, indicated a greater likelihood of e-cig use in asthmatics as compared to their non-asthmatic peers. Availability of different flavorings is often cited as the main reason among youth/adolescents for trying e-cigs or switching from cigarettes to e-cigs. Occupational inhalation of some common food-safe flavoring agents is reported to cause occupational asthma and worsen asthmatic symptoms. Moreover, workplace inhalation exposures to the flavoring agent diacetyl have caused irreversible obstructive airway disease in healthy workers. Additionally, recent studies report that thermal decomposition of propylene glycol (PG) and vegetable glycerin (VG), the base constituents of e-liquids, produces reactive carbonyls, including acrolein, formaldehyde, and acetaldehyde, which have known respiratory toxicities. Furthermore, recent nicotine studies in rodents reveal that prenatal nicotine exposures lead to epigenetic reprogramming in the offspring, abnormal lung development, and multigenerational transmission of asthmatic-like symptoms. Summary Comparisons of the toxicity and health effects of e-cigs and conventional cigarettes often focus on toxicants known to be present in cigarette smoke (CS) (i.e., formaldehyde, nitrosamines, etc.), as well as smoking-associated clinical endpoints, such as cancer, bronchitis, and chronic obstructive pulmonary disease (COPD). However, this approach disregards potential toxicity of components unique to flavored e-cigs, such as PG, VG, and the many different flavoring chemicals, which likely induce respiratory effects not usually observed in cigarette smokers.

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Nicotine alters mucin rheological properties

Cited by 31 publications

References 59 publications

Chronic electronic cigarette exposure in mice induces features of COPD in a nicotine-dependent manner

Chronic electronic cigarette exposure in mice induces features of COPD in a nicotine-dependent manner

Association of Gallbladder Mucocele Histologic Diagnosis with Selected Drug Use in Dogs: A Matched Case‐Control Study

Electronic Cigarettes: Their Constituents and Potential Links to Asthma

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