Lipopolysaccharide accelerates fine particulate matter-induced cell apoptosis in human lung bronchial epithelial cells

Ru, Qin; Xiong, Qi; Chen, Lin; Xiang, Tian; Yue, Kai; Ma, Baomiao; Liu, Lu; Wu, Rihui; Xu, Congyue; Pi, Min; Li, Chaoying

doi:10.13075/ijomeh.1896.00527

Cited by 6 publications

(6 citation statements)

References 23 publications

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“…Prague PM10 has been chemically characterised and was used to compare the Malmö PM chemical composition analysis undertaken in this study, and to test their biological activity on human trophoblast cells. Apoptosis and increased levels of reactive oxygen species following exposure of human bronchial epithelial cells to Prague PM10 (up to 500 μg/ml) has been reported [35].…”

Section: Methodsmentioning

confidence: 99%

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Exposure of trophoblast cells to fine particulate matter air pollution leads to growth inhibition, inflammation and ER stress

et al. 2019

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Ambient air pollution is considered a major environmental health threat to pregnant women. Our previous work has shown an association between exposure to airborne particulate matter (PM) and an increased risk of developing pre-eclamspia. It is now recognized that many pregnancy complications are due to underlying placental dysfunction, and this tissue plays a pivotal role in pre-eclamspia. Recent studies have shown that PM can enter the circulation and reach the human placenta but the effects of PM on human placental function are still largely unknown. In this work we investigated the effects of airborne PM on trophoblast cells. Human, first trimester trophoblast cells (HTR-8/SV) were exposed to urban pollution particles (Malmö PM2.5; Prague PM10) for up to seven days in vitro and were analysed for uptake, levels of hCGβ and IL-6 secretion and proteomic analysis. HTR-8/SVneo cells rapidly endocytose PM within 30 min of exposure and particles accumulate in the cell in perinuclear vesicles. High doses of Prague and Malmö PM (500–5000 ng/ml) significantly decreased hCGβ secretion and increased IL-6 secretion after 48 h exposure. Exposure to PM (50 ng/ml) for 48h or seven days led to reduced cellular growth and altered protein expression. The differentially expressed proteins are involved in networks that regulate cellular processes such as inflammation, endoplasmic reticulum stress, cellular survival and molecular transport pathways. Our studies suggest that trophoblast cells exposed to low levels of urban PM respond with reduced growth, oxidative stress, inflammation and endoplasmic reticulum stress after taking up the particles by endocytosis. Many of the dysfunctional cellular processes ascribed to the differentially expressed proteins in this study, are similar to those described in PE, suggesting that low levels of urban PM may disrupt cellular processes in trophoblast cells. Many of the differentially expressed proteins identified in this study are involved in inflammation and may be potential biomarkers for PE.

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Section: Methodsmentioning

confidence: 99%

“…Both PM samples were provided as powdered material that required sonication for resuspension, which is standard procedure in air pollution studies using cultured cells [35, 37, 38]. To disperse PM in solution, samples were subjected to a two-step sonication in 0.5 ml of RPMI in 1.5 ml tubes (Eppendorf).…”

Section: Methodsmentioning

confidence: 99%

Exposure of trophoblast cells to fine particulate matter air pollution leads to growth inhibition, inflammation and ER stress

et al. 2019

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“…2786, is a fine atmospheric particulate matter with a mean particle diameter <4 μm; PM 4.0 was purchased from the European Virtual Institute for Speciation Analysis (EVISA, Gaithersburg, MD, USA). SRM 2786 is an analytical method for the determination of selected polycyclic aromatic hydrocarbons (PAHs), nitro-substituted PAHs (nitro-PAHs), polybrominated diphenyl ether (PBDE) congeners, hexabromocyclododecane (HBCD) isomers, sugars, polychlorinated dibenzo- p -dioxin (PCDD) and dibenzofuran (PCDF) congeners, inorganic constituents, and particle-size characteristics in atmospheric particulate material and similar matrices 47–49 . Detailed information about the PAHs, trace elements and inorganic constituents of PM 4.0 can be found in Supplementary Tables S1, S2 and S3, respectively.…”

Section: Methodsmentioning

confidence: 99%

Kefir peptides alleviate particulate matter <4 μm (PM4.0)-induced pulmonary inflammation by inhibiting the NF-κB pathway using luciferase transgenic mice

Chen

Hung

Yen

et al. 2019

Sci Rep

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Kefir peptides, generated by kefir grain fermentation of milk proteins, showed positive antioxidant effects, lowered blood pressure and modulated the immune response. In this study, kefir peptide was evaluated regarding their anti-inflammatory effects on particulate matter <4 μm (PM 4.0 )-induced lung inflammation in NF-κB-luciferase +/+ transgenic mice. The lungs of mice under 20 mg/kg or 10 mg/kg PM 4.0 treatments, both increased significantly the generation of reactive oxygen species (ROS) and inflammatory cytokines; increased the protein expression levels of p-NF-κB, NLRP3, caspase-1, IL-1β, TNF-α, IL-6, IL-4 and α-SMA. Thus, we choose the 10 mg/kg of PM 4.0 for animal trials; the mice were assigned to four treatment groups, including control group (saline treatment), PM 4.0 + Mock group (only PM 4.0 administration), PM 4.0 + KL group (PM 4.0 + 150 mg/kg low-dose kefir peptide) and PM 4.0 + KH group (PM 4.0 + 500 mg/kg high-dose kefir peptide). Data showed that treatment with both doses of kefir peptides decreased the PM 4.0 -induced inflammatory cell infiltration and the expression of the inflammatory mediators IL-lβ, IL-4 and TNF-α in lung tissue by inactivating NF-κB signaling. The oral administrations of kefir peptides decrease the PM 4.0 -induced lung inflammation process through the inhibition of NF-κB pathway in transgenic luciferase mice, proposing a new clinical application to particulate matter air pollution-induced pulmonary inflammation.

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“…32,55 Along with the diffusion or import of ROS from airway surface lining fluid, air pollution exposure also stimulates intracellular ROS production. Many recent in vitro studies have examined the effect of various models of air pollution, which include ambient outdoor pollution around the world collected on filters, 11,45,48,49,[52][53][54][56][57][58][59][60] fresh traffic-related air pollution generated by gasoline or diesel engines, [19][20][21]50,51,61 SRMs, 26,62,63 and fresh wood smoke, [64][65][66][67] and have observed dose-and exposure-dependent increases in intracellular ROS or associated oxidation of proteins or DNA.…”

Section: Intracellular Responses: Oxidative Stressmentioning

confidence: 99%

An update on immunologic mechanisms in the respiratory mucosa in response to air pollutants

Huff

Carlsten

Hirota

2019

Journal of Allergy and Clinical Immunology

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Every day, we breathe in more than 10,000 L of air that contains a variety of air pollutants that can pose negative consequences to lung health. The respiratory mucosa formed by the airway epithelium is the first point of contact for air pollution in the lung, functioning as a mechanical and immunologic barrier. Under normal circumstances, airway epithelial cells connected by tight junctions secrete mucus, airway surface lining fluid, host defense peptides, and antioxidants and express innate immune pattern recognition receptors to respond to inhaled foreign substances and pathogens. Under conditions of air pollution exposure, the defenses of the airway epithelium are compromised by reductions in barrier function, impaired host defense to pathogens, and exaggerated inflammatory responses. Central to the mechanical and immunologic changes induced by air pollution are activation of redox-sensitive pathways and a role for antioxidants in normalizing these negative effects. Genetic variants in genes important in epithelial cell function and phenotype contribute to a diversity of responses to air pollution in the population at the individual and group levels and suggest a need for personalized approaches to attenuate the respiratory mucosal immune responses to air pollution.

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Lipopolysaccharide accelerates fine particulate matter-induced cell apoptosis in human lung bronchial epithelial cells

Cited by 6 publications

References 23 publications

Exposure of trophoblast cells to fine particulate matter air pollution leads to growth inhibition, inflammation and ER stress

Exposure of trophoblast cells to fine particulate matter air pollution leads to growth inhibition, inflammation and ER stress

Kefir peptides alleviate particulate matter <4 μm (PM4.0)-induced pulmonary inflammation by inhibiting the NF-κB pathway using luciferase transgenic mice

An update on immunologic mechanisms in the respiratory mucosa in response to air pollutants

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