Cigarette-smoke-induced priming of neutrophils from smokers and non-smokers for increased oxidative burst response is mediated by TNF-α

Friedrichs, Bärbel; Neumann, Ute; Schüller, Jutta; Peck, Michael J.

doi:10.1016/j.tiv.2014.06.007

Cited by 23 publications

(14 citation statements)

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“…TNF-α also increased low-density lipoprotein uptake in vascular endothelium in vitro, a process known to promote atherosclerosis and further proinflammatory signalling (figure 2e) [40]. In patients with COPD, the influx of leukocytes into the lungs contributes to lung damage through protease and ROS, a process which TNF-α can enhance, further contributing to damage [121]. Furthermore, TNF-α increased the susceptibility of pulmonary vascular endothelium to ROS in vitro by reducing glutathione levels intracellularly, presenting a mechanism of enhanced damage of pulmonary endothelium in oxidative environments (figure 2a) [122].…”

Section: Evidence For Overspillmentioning

confidence: 99%

“…There are clear links with altered cellular functions, inflammation and senescence, with impaired immune cell surveillance associated with a higher burden of senescent cells [157], a greater burden of SASP and the associated systemic and tissue inflammation [36,41,112]. Once present, inflammation, including TNF-α, serves as an important priming agent for the oxidative burst [121]. ROS can damage cells and tissues, instigate further proinflammatory responses and exacerbate DNA damage.…”

Section: Interwoven Processes Require An Integrated Approachmentioning

confidence: 99%

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Shared mechanisms of multimorbidity in COPD, atherosclerosis and type-2 diabetes: the neutrophil as a potential inflammatory target

2020

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Multimorbidity is increasingly common and current healthcare strategies are not always aligned to treat this complex burden of disease. COPD, type-2 diabetes mellitus (T2D) and cardiovascular disease, especially atherosclerosis, occur more frequently together than expected, even when risk factors such as smoking, obesity, inactivity and poverty are considered. This supports the possibility of unifying mechanisms that contribute to the pathogenesis or progression of each condition.Neutrophilic inflammation is causally associated with COPD, and increasingly recognised in the pathogenesis of atherosclerosis and T2D, potentially forming an aetiological link between conditions. This link might reflect an overspill of inflammation from one affected organ into the systemic circulation, exposing all organs to an increased milieu of proinflammatory cytokines. Additionally, increasing evidence supports the involvement of other processes in chronic disease pathogenesis, such as cellular senescence or changes in cellular phenotypes.This review explores the current scientific evidence for inflammation, cellular ageing and cellular processes, such as reactive oxygen species production and phenotypic changes in the pathogenesis of COPD, T2D and atherosclerosis; highlighting common mechanisms shared across these diseases. We identify emerging therapeutic approaches that target these areas, but also where more work is still required to improve our understanding of the underlying cellular biology in a multimorbid disease setting.

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Section: Evidence For Overspillmentioning

confidence: 99%

Section: Interwoven Processes Require An Integrated Approachmentioning

confidence: 99%

Shared mechanisms of multimorbidity in COPD, atherosclerosis and type-2 diabetes: the neutrophil as a potential inflammatory target

2020

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“…For example, TNFα—shown to be increased in airway secretions from patients with COPD, asthma, bronchiectasis and AATD—is able to increase the expression of capture receptors and adhesion molecules on the surface of blood vascular endothelial cells, enhancing neutrophil migration into the inflamed lung 146 . Furthermore, TNFα can impact on cellular functions as it is a potent priming agent and able to increase ROS production by neutrophils, which will further contribute to tissue damage 147 . Second (and more speculatively), the inflammation present across diseases might impair the ability of the lungs to “de-prime” cells 29 , leading to a circulating population of primed cells, which might confer a more aggressive cellular phenotype.…”

Section: Common Mechanisms Across Diseasesmentioning

confidence: 99%

Understanding the role of neutrophils in chronic inflammatory airway disease

et al. 2019

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Airway neutrophilia is a common feature of many chronic inflammatory lung diseases and is associated with disease progression, often regardless of the initiating cause. Neutrophils and their products are thought to be key mediators of the inflammatory changes in the airways of patients with chronic obstructive pulmonary disease (COPD) and have been shown to cause many of the pathological features associated with disease, including emphysema and mucus hypersecretion. Patients with COPD also have high rates of bacterial colonisation and recurrent infective exacerbations, suggesting that neutrophil host defence mechanisms are impaired, a concept supported by studies showing alterations to neutrophil migration, degranulation and reactive oxygen species production in cells isolated from patients with COPD. Although the role of neutrophils is best described in COPD, many of the pathological features of this disease are not unique to COPD and also feature in other chronic inflammatory airway diseases, including asthma, cystic fibrosis, alpha-1 anti-trypsin deficiency, and bronchiectasis. There is increasing evidence for immune cell dysfunction contributing to inflammation in many of these diseases, focusing interest on the neutrophil as a key driver of pulmonary inflammation and a potential therapeutic target than spans diseases. This review discusses the evidence for neutrophilic involvement in COPD and also considers their roles in alpha-1 anti-trypsin deficiency, bronchiectasis, asthma, and cystic fibrosis. We provide an in-depth assessment of the role of the neutrophil in each of these conditions, exploring recent advances in understanding, and finally discussing the possibility of common mechanisms across diseases.

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“…Upon exposure to cigarette smoke and the bacterial peptide N-formylmethionyl-leucyl-phenalanine (fMLP), neutrophils increase the expression of CD11b and CD66b, important for the migration and degranulation of neutrophils at sites of inflammation [ 20 , 21 ]. There is increased expression of the adhesion molecule CD11b on the surface of blood and lung neutrophils of COPD patients [ 22 – 25 ].…”

Section: Introductionmentioning

confidence: 99%

Electronic cigarette exposure triggers neutrophil inflammatory responses

Higham¹,

Rattray

Dewhurst³

et al. 2016

Respir Res

127

104

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BackgroundThe use of electronic cigarettes (e-cigs) is increasing and there is widespread perception that e-cigs are safe. E-cigs contain harmful chemicals; more research is needed to evaluate the safety of e-cig use. Our aim was to investigate the effects of e-cigs on the inflammatory response of human neutrophils.MethodsNeutrophils were exposed to e-cig vapour extract (ECVE) and the expression of CD11b and CD66b was measured by flow cytometry and MMP-9 and CXCL8 by ELISA. We also measured the activity of neutrophil elastase (NE) and MMP-9, along with the activation of inflammatory signalling pathways. Finally we analysed the biochemical composition of ECVE by ultra-high performance liquid chromatography mass spectrometry.ResultsECVE caused an increase in the expression of CD11b and CD66b, and increased the release of MMP-9 and CXCL8. Furthermore, there was an increase in NE and MMP-9 activity and an increase in p38 MAPK activation. We also identified several harmful chemicals in ECVE, including known carcinogens.ConclusionsECVE causes a pro-inflammatory response from human neutrophils. This raises concerns over the safety of e-cig use.Electronic supplementary materialThe online version of this article (doi:10.1186/s12931-016-0368-x) contains supplementary material, which is available to authorized users.

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Cigarette-smoke-induced priming of neutrophils from smokers and non-smokers for increased oxidative burst response is mediated by TNF-α

Cited by 23 publications

References 50 publications

Shared mechanisms of multimorbidity in COPD, atherosclerosis and type-2 diabetes: the neutrophil as a potential inflammatory target

Shared mechanisms of multimorbidity in COPD, atherosclerosis and type-2 diabetes: the neutrophil as a potential inflammatory target

Understanding the role of neutrophils in chronic inflammatory airway disease

Electronic cigarette exposure triggers neutrophil inflammatory responses

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