Oxidative stress-mediated epidermal growth factor receptor activation regulates PM2.5-induced over-secretion of pro-inflammatory mediators from human bronchial epithelial cells.
Biochim Biophys Acta Gen Subj
; 1864(10): 129672, 2020 10.
Article
in English
| MEDLINE | ID: covidwho-601229
ABSTRACT
BACKGROUND:
Exposure to PM2.5 has been associated with increased morbidity and mortality of lung diseases although the underlying mechanisms have not been fully uncovered. Airway inflammation is a critical event in the pathogenesis of lung diseases. This study aimed to examine the role of oxidative stress and epidermal growth factor receptor (EGFR) in PM2.5-induced pro-inflammatory response in a human bronchial epithelial cell line, BEAS-2B.METHODS:
BEAS-2B cells were exposed to 0, 20, 50, 100 and 150 µg/ml of PM2.5. Secretion of pro-inflammatory mediators including interleukin-6 (IL-6), IL-8 and IL-1ß was determined using enzyme linked immunosorbent assay. Levels of intracellular reactive oxygen species (ROS) were determined using flow cytometry. Phosphorylation of the EGFR was examined with immunoblotting.RESULTS:
PM2.5 exposure increased the secretion of IL-6, IL-8, and IL-1ß in a concentration-dependent fashion. Moreover, exposure to PM2.5 elevated intracellular levels of ROS, and phosphorylation of the EGFR (Y1068). Pretreatment of BEAS-2B cells with either an antioxidant or a specific EGFR inhibitor significantly reduced PM2.5-induced IL-6, IL-8 and IL-1ß secretion, implying that both oxidative stress and EGFR activation were involved in PM2.5-induced pro-inflammatory response. Furthermore, pre-treatment of BEAS-2B cells with an antioxidant significantly blunted PM2.5-induced EGFR activation, suggesting that oxidative stress was required for PM2.5-induced EGFR activation.CONCLUSION:
PM2.5 exposure induces pro-inflammatory response in human bronchial epithelial cells through oxidative stress-mediated EGFR activation.Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Oxidative Stress
/
Inflammation Mediators
/
Air Pollutants
/
Epithelial Cells
/
Particulate Matter
Limits:
Humans
Language:
English
Journal:
Biochim Biophys Acta Gen Subj
Year:
2020
Document Type:
Article
Affiliation country:
J.bbagen.2020.129672
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