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

2014 ◽  
Vol 31 (8) ◽  
pp. 923-936 ◽  
Author(s):  
Lawei Yang ◽  
Gang Liu ◽  
Ziying Lin ◽  
Yahong Wang ◽  
Huijuan He ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Particulate Matter ◽  
Epithelial Cells ◽  
Inflammatory Response ◽  
Bronchial Epithelial Cells ◽  
Ambient Particulate Matter ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
And Oxidative Stress

scholarly journals Effects of vitamin D on inflammatory and oxidative stress responses of human bronchial epithelial cells exposed to particulate matter

2018 ◽  
Author(s):  
Paul E Pfeffer ◽  
Haw Lu ◽  
Elizabeth H Mann ◽  
Yin-Huai Chen ◽  
Tzer-Ren Ho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Particulate Matter ◽  
Epithelial Cells ◽  
Transcriptome Analysis ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Altered Expression ◽  
Bronchial Epithelial ◽  
And Oxidative Stress

AbstractBackgroundParticulate matter (PM) pollutant exposure, which induces oxidative stress and inflammation, and vitamin D insufficiency, which compromises immune regulation, are detrimental in asthma.ObjectivesMechanistic cell culture experiments were undertaken to ascertain whether vitamin D abrogates PM-induced inflammatory responses of human bronchial epithelial cells (HBECs) through enhancement of antioxidant pathways.MethodsTranscriptome analysis, PCR and ELISA were undertaken to delineate markers of inflammation and oxidative stress; with comparison of expression in primary HBECs from healthy and asthmatic donors cultured with reference urban PM in the presence/absence of vitamin D.ResultsTranscriptome analysis identified over 500 genes significantly perturbed by PM-stimulation, including multiple pro-inflammatory cytokines. Vitamin D altered expression of a subset of these PM-induced genes, including suppressing IL6. Addition of vitamin D suppressed PM-stimulated IL-6 production, although to significantly greater extent in healthy versus asthmatic donor cultures. Vitamin D also differentially affected PM-stimulated GM-CSF, with suppression in healthy HBECs and enhancement in asthmatic cultures. Vitamin D increased HBEC expression of the antioxidant pathway gene G6PD, increased the ratio of reduced to oxidised glutathione, and in PM-stimulated cultures decreased the formation of 8-isoprostane. Pre-treatment with vitamin D decreased CXCL8 and further decreased IL-6 production in PM-stimulated cultures, an effect abrogated by inhibition of G6PD with DHEA, supporting a role for this pathway in the anti-inflammatory actions of vitamin D.ConclusionsIn a study using HBECs from 18 donors, vitamin D enhanced HBEC antioxidant responses and modulated the immune response to PM, suggesting that vitamin D may protect the airways from pathological pollution-induced inflammation.

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