The role of IL-6 released from pulmonary epithelial cells in diesel UFP-induced endothelial activation

Bengalli, Rossella; Longhin, Eleonora; Marchetti, Sara; Proverbio, Maria Carla; Battaglia, Cristina; Camatini, Marina

doi:10.1016/j.envpol.2017.08.104

Cited by 15 publications

(21 citation statements)

References 42 publications

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“…When HBEC, derived from immortalized cell lines or normal donors, are exposed to ambient PM or DEPs, a strong up‐regulation of different epithelial cytokines can be observed. The levels of IL‐6, IL‐8 and TNF‐α, for instance, were significantly increased in cells that were exposed to PM. Of note, also MIP‐3α/CCL20, an important chemokine involved in DC recruitment, was increased in HBEC upon ambient PM exposure.…”

Section: Air Pollution and Asthmamentioning

confidence: 99%

“…When lung epithelial cells are exposed to ambient PM/DEPs higher levels of intracellular ROS formation, activation of oxidative stress‐responsive genes, such as HMOX1, and oxidative damage has been demonstrated . Ambient PM/DEPs exposure was further associated with the overexpression of several genes and increased phosphorylated proteins related to the MAPK or PI3K/AKT pathway . Several studies also demonstrated that PM activates NF‐ κB signalling in airway epithelial cells to induce inflammation …”

Section: Air Pollution and The Airway Epitheliummentioning

confidence: 99%

“…Importantly, after internalization or PRR activation, exposure to ambient PM/DEPs will activate oxidative stress responses in the airway epithelial cells. When lung epithelial cells are exposed to ambient PM/DEPs higher levels of intracellular ROS formation, activation of oxidative stress‐responsive genes, such as HMOX1, and oxidative damage has been demonstrated . Ambient PM/DEPs exposure was further associated with the overexpression of several genes and increased phosphorylated proteins related to the MAPK or PI3K/AKT pathway .…”

Section: Air Pollution and The Airway Epitheliummentioning

confidence: 99%

“…Although it is clear that DEPs and PM can up‐regulate the expression of numerous pro‐inflammatory epithelial cytokines, not all studies reported an altered cytokine expression . Differences in epithelial responses can be explained by variations in chemical composition, more specifically by the amount of adsorbed organic compounds, metals and presence of endotoxins on the particle's surface.…”

Section: Air Pollution and Asthmamentioning

confidence: 99%

“…Although it is clear that DEPs and PM can up-regulate the expression of numerous pro-inflammatory epithelial cytokines, not all studies reported an altered cytokine expression. 70,72,75,139 Differences in epithelial responses can be explained by variations in chemical composition, more specifically by the amount of adsorbed organic compounds, metals and presence of endotoxins on the particle's surface. By extracting ambient PM or DEPs, for instance, it was demonstrated that especially the organic compounds were the main contributors to epithelial IL-1b, IL-6, IL-8 and GM-CSF release.…”

Section: Particulate Matter and Epithelial Cytokine Expression: Hummentioning

confidence: 99%

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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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Section: Air Pollution and Asthmamentioning

confidence: 99%

Section: Air Pollution and The Airway Epitheliummentioning

confidence: 99%

Section: Air Pollution and The Airway Epitheliummentioning

confidence: 99%

Section: Air Pollution and Asthmamentioning

confidence: 99%