Interleukins 6/8 and cyclooxygenase‐2 release and expressions are regulated by oxidative stress‐JAK2/STAT3 signaling pathway in human bronchial epithelial cells exposed to particulate matter ≤2.5 μm

2020 ◽  
Vol 40 (9) ◽  
pp. 1210-1218 ◽  
Author(s):  
Zhenzhen Xu ◽  
Hongyan Wu ◽  
Hongmei Zhang ◽  
Jianying Bai ◽  
Zhihong Zhang
Keyword(s):  
Oxidative Stress ◽  
Particulate Matter ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Particulate Matter 2.5

scholarly journals Sappanone A inhibits oxidative stress, inflammation and apoptosis in cigarette smoke-induced human bronchial epithelial cells through regulating Nrf2/HO-1 and TLR4/NF-κB signaling pathways

2020 ◽  
Author(s):  
Yan Zhang ◽  
Shanshan Wang ◽  
Hongli Li ◽  
Xia Xu
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Cigarette Smoke ◽  
Bronchial Epithelial Cells ◽  
Chronic Obstructive ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial

Abstract Chronic obstructive pulmonary disease (COPD) is a common respiratory disease associated with inflammation and oxidative stress. Sappanone A (SA) is a homoisoflavanone that has been proven to have anti-inflammatory and anti-oxidant effects. However, the role of SA in COPD remains unclear. Thus, the present study was aimed to evaluate the beneficial effect of SA on COPD in vitro. The human bronchial epithelial cells were exposed to 5% cigarette smoke extracts (CSE) to induce an in vitro model of COPD. Our results showed that SA treatment significantly attenuated the CSE-caused induction of ROS and reduction of SOD and GPx activities in 16HBE cells. In addition, SA inhibited the production of inflammatory cytokines IL-6, IFN-γ, and TNF-α in CSE-stimulated 16HBE cells. Moreover, the CSE-stimulated cell apoptosis of 16HBE cells were abrogated by SA. Furthermore, we observed that SA treatment greatly promoted the activation of Nrf2/HO-1 signaling pathway, as well as inhibited the activation of TLR4/NF-κB signaling pathway in CSE-stimulated 16HBE cells. Subsequent rescue assay revealed that the protective effects of SA on CSE-stimulated 16HBE cells were reversed by Nrf2 knockdown or TLR4 overexpression. Taken together, these findings demonstrated that SA inhibits oxidative stress, inflammation and apoptosis in CSE-induced human bronchial epithelial cells through regulating Nrf2/HO-1 and TLR4/NF-κB signaling pathways.

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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