E-cigarette vapour enhances pneumococcal adherence to airway epithelial cells

Miyashita, Lisa; Suri, Reetika; Dearing, Emma; Mudway, Ian; Dove, Rosamund; Neill, Daniel R.; Zyl-Smit, Richard van; Kadioglu, Aras; Grigg, Jonathan

doi:10.1183/13993003.01592-2017

Cited by 119 publications

(110 citation statements)

References 29 publications

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“…82 The increased levels of nasal PAFR were seen in adults inhaling E-cigarette vapour for 5 minutes. 83 ECVE (with or without nicotine) also increase pneumococcal adhesion to a human epithelial cell line, and this was related to ROS production. Since pneumococcal infection is the commonest cause of bacterial pneumonia, E-cigarette use has the potential to facilitate pneumococcal diseases.…”

Section: Effects Of E-cigarettes On Resistance To Infectionmentioning

confidence: 91%

“…Platelet‐activating factor receptor (PAFR) is used by pneumococci to adhere to host cells, and CS increases pneumococcal adhesion by up‐regulating PAFR expression in human lower epithelial cells (Table ) . The increased levels of nasal PAFR were seen in adults inhaling E‐cigarette vapour for 5 minutes . ECVE (with or without nicotine) also increase pneumococcal adhesion to a human epithelial cell line, and this was related to ROS production.…”

Section: Effects Of E‐cigarettes In Humansmentioning

confidence: 99%

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Immunological and pathological effects of electronic cigarettes

Chen

Todd

Fairclough

2019

Basic Clin Pharma Tox

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Electronic cigarettes (E‐cigarettes) are considered a preferable alternative to conventional cigarettes due to the lack of combustion and the absence of tobacco‐specific toxicants. E‐cigarettes have rapidly gained in popularity in recent years amongst both existing smokers and previous non‐smokers. However, a growing literature demonstrates that E‐cigarettes are not as safe as generally believed. Here, we discuss the immunological, and other, deleterious effects of E‐cigarettes on a variety of cell types and host defence mechanisms in humans and in murine models. We review not only the effects of complete E‐cigarette liquids, but also each of the main components—nicotine, humectants and flavourings. This MiniReview thus highlights the possible role of E‐cigarettes in the pathogenesis of disease and raises awareness of the potential harm that E‐cigarettes may cause.

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Section: Effects Of E-cigarettes On Resistance To Infectionmentioning

confidence: 91%

Section: Effects Of E‐cigarettes In Humansmentioning

confidence: 99%

Immunological and pathological effects of electronic cigarettes

Chen

Todd

Fairclough

2019

Basic Clin Pharma Tox

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“…62 Notably, PAFR expression is increased in response to environmental exposures, in particular CS, air pollution, acids, viral infections, 60,63 welding fumes 64 and e-cigarette vapour. 65 Crucially, PAFR protein is increased in the large and small airways of COPD patients and correlates with current and previous smoking history. 51,66 The bacterial adhesion enabled by the PAFR is directly linked to increased susceptibility to infection by both Gram-positive and Gram-negative bacteria.…”

Section: Role Of Pafr In Bacterial Persistencementioning

confidence: 99%

“…Although little is known of the effects of PAF itself in the airways, the PAFR plays crucial roles in biological processes, including vasodilation, cell proliferation and angiogenesis, and in regulating inflammatory responses . Notably, PAFR expression is increased in response to environmental exposures, in particular CS, air pollution, acids, viral infections, welding fumes and e‐cigarette vapour . Crucially, PAFR protein is increased in the large and small airways of COPD patients and correlates with current and previous smoking history .…”

Section: Bacterial Colonization and Infection In Copdmentioning

confidence: 99%

Hypoxia‐inducible factor and bacterial infections in chronic obstructive pulmonary disease

et al. 2019

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COPD is a seriously disabling respiratory condition that inexorably progresses to disability and mortality. It affects approximately 10% of the population globally with a greater prevalence at advanced ages. Airway bacterial infections complicate the disease course in most COPD patients, leading to increased symptoms, more rapid decline in lung function, acute exacerbations and reduced quality of life. With increasing bacterial resistance to antibiotics and adverse effects of conventional treatments, new effective non‐antibiotic antimicrobial therapies are urgently needed to manage COPD. Hypoxia‐inducible factor (HIF)‐1α is an important transcriptional regulator of cellular responses to hypoxia, oxidants and inflammation, and is overexpressed in the lungs of COPD patients. Recent evidence shows that increased HIF‐1α expression can upregulate the platelet‐activating factor receptor (PAFR) on the airway epithelial surface that is increased in smokers and particularly COPD patients. The receptor is utilized by PAFR‐dependent bacteria (Streptococcus pneumoniae, Haemophilus influenzae and Pseudomonas aeruginosa) to induce infection in both the respiratory and gastrointestinal (GI) tracts. However, the importance and mechanism of HIF‐1α in augmenting PAFR‐dependent bacterial infections in COPD are poorly understood. Here, we review the evidence for the roles of local tissue hypoxia‐induced inflammation, HIF‐1α and PAFR in facilitating bacterial infections in COPD. Blocking PAFR may provide a novel antimicrobial approach to manage bacterial infections in COPD.

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“…The exposure to EV was shown to induce biofilm formation, hydrophobicity, and adherence to epithelial cells by S. aureus [20]. In another study, EV exposure was shown to facilitate pneumococcal host epithelial adherence via significant upregulation of platelet activating factor receptor (PAFR) in nasal epithelial cells from vapers, as well as in EV-exposed A549 lung carcinoma cell line [21]. Notably, the effects of EV exposure on the transcriptome and the pathogenesis of S. pneumoniae are largely undefined.…”

Section: Introductionmentioning

confidence: 99%

The effects of e-cigarette vapor exposure on the transcriptome and virulence of Streptococcus pneumoniae

Bagale

Paudel

Cagle

et al. 2019

Preprint

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14The effects of e-cigarette vapor (EV) exposure on the physiology of respiratory microflora are 15 not fully defined. We analyzed the effects of exposure to vapor from nicotine-containing and 16 nicotine-free e-liquid formulations on virulence and transcriptome of Streptococcus pneumoniae 17 strain TIGR4, a pathogen that asymptomatically colonizes human nasopharyngeal mucosa. 18 TIGR4 was pre-exposed for 2h to nicotine-containing EV extract (EVE+NIC), nicotine-free EV 19 extract (EVE-NIC), cigarette smoke extract (CSE), or nutrient-rich TS broth (control). The 20 differences in the treatment and control TIGR4 were explored using transcriptome sequencing, in 21 vitro virulence assays, and in vivo mouse model of acute pneumonia. The analysis of RNASeq 22 Importance 37With the increasing popularity of e-cigarettes amongst cigarette smoking and non-smoking 38 adults and children, and the recent reports of vaping related lung illnesses and deaths, further 39 analysis of the adverse health effects of e-cigarette vapor (EV) exposure is warranted. Since 40 pathogenic bacteria such as Streptococcus pneumoniae can colonize the human nasopharynx as 41 commensals, they may be affected by the exposure to bioactive chemicals in EV. Hence in this 42 study we examined the effects of EV exposure on the physiology of S. pneumoniae strain 43 TIGR4. In order to differentiate between the effects of nicotine and non-nicotine components, we 44 specifically compared RNASeq profiles and virulence of TIGR4 exposed to vapor from nicotine-45 containing and nicotine-free e-liquid formulations. We observed that nicotine-containing EV 46 augmented TIGR4 biofilms and altered expression of TIGR4 genes predominantly involved in 47 metabolism and stress response. However, neither nicotine-containing nor nicotine-free EV 48 affected TIGR4 virulence in a mouse model. 49 words 50 51The e-cigarette is a handheld device that electronically heats an e-liquid and generates 52 aerosolized e-cigarette vapor (EV) that is inhaled by the user. Originally, e-cigarettes were 53 marketed as a safer alternative to smoking and as an effective smoking cessation device. 54Contrary to these claims, emerging research has repeatedly demonstrated the adverse health 55 effects of EV exposure, and in the last decade the number of new e-cigarette users (vapers) and 56 cigarette smokers who also use e-cigarette (dual users) has increased at a rapid pace. Currently, 57 the exploding popularity of e-cigarette use (vaping) is threatening the success of various public 58 health campaigns to reduce cigarette smoking. Especially worrisome is the rise in vaping 59 amongst the youth and teenagers. In 2018, 4.9% of middle school and 20.8% of high school 60 students (~3.6 million total) in the USA reported vaping [1]. Commercially available e-liquids 61 typically contain three main ingredients: 1) a vehicle mixture of the humectants propylene glycol 62 and/or vegetable glycerin which determines vapor density and throat hit intensity; 2) flavoring 63 chemicals such as cinnamaldehyde,...

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E-cigarette vapour enhances pneumococcal adherence to airway epithelial cells

Cited by 119 publications

References 29 publications

Immunological and pathological effects of electronic cigarettes

Immunological and pathological effects of electronic cigarettes

Hypoxia‐inducible factor and bacterial infections in chronic obstructive pulmonary disease

The effects of e-cigarette vapor exposure on the transcriptome and virulence of Streptococcus pneumoniae

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