Pro‐inflammatory response and oxidative stress induced by specific components in ambient particulate matter in human bronchial epithelial cells

Yang, Liting; Liu, Gang; Lin, Ziying; Wang, Yahong; Huang, He; Li, Shipeng; Kamp, David W.

doi:10.1002/tox.22102

Cited by 99 publications

(53 citation statements)

References 43 publications

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“…Number sign indicates that the value was significantly different when compared to that of the nanoparticle treatment (P<0.05) and cytokines [23,39]. Our results showed that nanoparticles, but not fine particles of WC-Co at 5 μg/cm 2 stimulate ROS production.…”

Section: Discussionsupporting

confidence: 51%

Tungsten Carbide-Cobalt Nanoparticles Induce Reactive Oxygen Species, AKT, ERK, AP-1, NF-κB, VEGF, and Angiogenesis

Liu

Ding

Zheng

et al. 2015

Biol Trace Elem Res

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Powder mixtures of tungsten carbide and metallic cobalt (WC-Co) are widely used in various products. Nanoparticles are engineered structures with at least one dimension of 100 nm or smaller. WC-Co is known to be associated with lung injury and diseases. Angiogenesis is a key process during vasculature, carcinogenesis, recovery of injury, and inflammatory diseases. However, the cellular effects of WC-Co nanoparticles on angiogenesis remain to be elucidated. In this study, we investigated angiogenic response and relative mechanisms after exposure to WC-Co nanoparticles. Our results showed that WC-Co nanoparticles at 5 μg/cm(2) induced ROS production which activated AKT and ERK1/2 signaling pathways in lung epithelial cells by reactive oxygen species (ROS) staining and immunoblotting; WC-Co treatment also increased transcriptional activation of AP-1, NF-κB, and VEGF by reporter assay. Further studies demonstrated that ROS are upstream molecules of AKT and ERK signaling pathways; the activation of AP-1, NF-κB, and VEGF was through ROS generation, AKT and ERK1/2 activation. In addition, WC-Co nanoparticles affected the cells to induce angiogenesis by chicken chorioallantoic membrane (CAM) assay. These results illustrate that exposure to WC-Co nanoparticles induces angiogenic response by activating ROS, AKT, and ERK1/2 signaling pathways and the downstream molecules and elucidate the potential molecular mechanisms during this process. This information may be useful for preventing potential damage from nanoparticle exposure in the future.

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Section: Discussionsupporting

confidence: 51%

Tungsten Carbide-Cobalt Nanoparticles Induce Reactive Oxygen Species, AKT, ERK, AP-1, NF-κB, VEGF, and Angiogenesis

Liu

Ding

Zheng

et al. 2015

Biol Trace Elem Res

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“…In addition, IL‐1 and granulocyte colony‐stimulating factor (GM‐CSF) have also been identified as important type 2‐promoting cytokines and were both increased in the bronchial epithelium of asthmatics . Interestingly, these typical type 2‐promoting cytokines, including, IL‐1α, IL‐1β, IL‐33, TSLP and GM‐CSF, were also increased in PM‐exposed normal HBEC. In contrast, IL‐25 levels were undetectable or decreased .…”

Section: Air Pollution and Asthmamentioning

confidence: 99%

“…Removal of surface‐bound endotoxins led to decreased cytokine responses, that is IL‐1α and GM‐CSF, implicating endotoxins in the PM‐induced epithelial cytokine release. In line, epithelial responses differed when sample collection was performed over different time periods or locations . Furthermore, epithelial cytokine expression can be influenced by the particle's size, as well as the experimental set‐up, the selected PM dose and epithelial cell culture …”

Section: Air Pollution and Asthmamentioning

confidence: 99%

Insights in particulate matter‐induced allergic airway inflammation: Focus on the epithelium

Grove

Provoost

Brusselle

et al. 2018

Clin Experimental Allergy

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Outdoor air pollution is a major environmental health problem throughout the world. In particular, exposure to particulate matter (PM) has been associated with the development and exacerbation of several respiratory diseases, including asthma. Although the adverse health effects of PM have been demonstrated for many years, the underlying mechanisms have not been fully identified. In this review, we focus on the role of the lung epithelium and specifically highlight multiple cytokines in PM-induced respiratory responses. We describe the available literature on the topic including in vitro studies, findings in humans (ie observations in human cohorts, human controlled exposure and ex vivo studies) and in vivo animal studies. In brief, it has been shown that exposure to PM modulates the airway epithelium and promotes the production of several cytokines, including IL-1, IL-6, IL-8, IL-25, IL-33, TNF-α, TSLP and GM-CSF. Further, we propose that PM-induced type 2-promoting cytokines are important mediators in the acute and aggravating effects of PM on airway inflammation. Targeting these cytokines could therefore be a new approach in the treatment of asthma.

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“…The PM 2.5 suspensions were vortexed and stored at 4˚C. PM 2.5 filter samples were analyzed according to a previous study (15), the results of which are exhibited in Table I.…”

Section: Introductionmentioning

confidence: 99%

Particulate matter 2.5 induces autophagy via inhibition of the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin kinase signaling pathway in human bronchial epithelial cells

Wang

et al. 2015

Molecular Medicine Reports

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Abstract. Particulate matter 2.5 (PM 2.5 ) is a significant risk factor for asthma. A recent study revealed that autophagy was associated with asthma pathogenesis. However, the specific mechanisms underlying PM 2.5 -induced autophagy in asthma have remained elusive. In the present study, PM 2.5 -induced autophagy was evaluated in Beas-2B human bronchial epithelial cells and the potential molecular mechanisms were investigated. Using electron microscopy, immunofluorescence staining and immunoblot studies, it was confirmed that PM 2.5 induced autophagy in Beas-2B cells as a result of PM 2.5 -mediated inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway in Beas-2B cells. LY294002, a PI3K inhibitor, reduced the accumulation of microtubule-associated protein 1 light chain 3 II and attenuated the effect of PM 2.5 . Phosphorylated (p-)p38, p-extracellular signal-regulated kinase and p-c-Jun N-terminal kinase were dephosphorylated following exposure to PM 2.5 . The roles of p53, reactive oxygen species scavenger tetramethylthiourea and autophagy inhibitor 3-methyladenine in PM 2.5 -induced autophagy in Beas-2B cells were also investigated. The results suggested that the PI3K/Akt/mTOR signaling pathway may be a key contributor to PM 2.5 -induced autophagy in Beas-2B cells. The results of the present study therefore provided an a insight into potential future clinical applications targeting these signaling pathways, for the prevention and/or treatment of PM 2.5 -induced lung diseases. IntroductionAcute and chronic exposure to particulate matter (PM), particularly fine particles with aerodynamic diameters of ≤2.5 µm PM 2.5 , has been shown to increase the number of hospital admissions for respiratory causes amongst the general population (1). Evidence obtained from environmental and epidemiological studies has revealed a marked association between fine particulate air pollution and multiple health issues, including respiratory illnesses (for example, respiratory track inflammation, asthma, acute bronchitis and lung cancer) as well as cardiovascular disease mortality (2-4).Increasing evidence supporting a link between traffic-associated air pollution and the incidence of childhood asthma has emerged; however, published estimates highlight the variability observed between populations (5,6). Asthma is a common worldwide respiratory symptom complex, frequently involving airway inflammation, which results in clinically significant physiological airway dysfunction. Asthma pathogenesis is complex, and multiple factors have roles in the development of the disease (7).Autophagy describes an evolutionarily conserved and tightly regulated lysosomal pathway, responsible for the degradation of macromolecules, including proteins, glycogen, lipids, nucleotides and organelles, via several complex pathways (8).Particulate matter 2.5 induces autophagy via inhibition of the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin kinase signaling pathway in human bronchial epithelial ...

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Pro‐inflammatory response and oxidative stress induced by specific components in ambient particulate matter in human bronchial epithelial cells

Cited by 99 publications

References 43 publications

Tungsten Carbide-Cobalt Nanoparticles Induce Reactive Oxygen Species, AKT, ERK, AP-1, NF-κB, VEGF, and Angiogenesis

Tungsten Carbide-Cobalt Nanoparticles Induce Reactive Oxygen Species, AKT, ERK, AP-1, NF-κB, VEGF, and Angiogenesis

Insights in particulate matter‐induced allergic airway inflammation: Focus on the epithelium

Particulate matter 2.5 induces autophagy via inhibition of the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin kinase signaling pathway in human bronchial epithelial cells

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