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Oxidative stress and endocytosis are involved in upregulation of interleukin‐8 expression in airway cells exposed to PM 2.5
Author(s) -
Yan Zhen,
Wang Jia,
Li Juan,
Jiang Nan,
Zhang Ruiqin,
Yang Weichao,
Yao Wu,
Wu Weidong
Publication year - 2016
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22188
Subject(s) - oxidative stress , endocytosis , reactive oxygen species , chemistry , downregulation and upregulation , cell culture , tumor necrosis factor alpha , microbiology and biotechnology , inflammation , biology , immunology , cell , biochemistry , genetics , gene
Inhaled PM2.5 (particulate matter with an aerodynamic diameter of 2.5 μm or less) can induce lung inflammation through released inflammatory mediators from airway cells, such as interleukin‐8 (IL‐8) and tumor necrosis factor alpha (TNF‐α). However, the mechanisms underlying PM2.5‐induced IL‐8 gene expression have not been fully characterized. BEAS‐2B cells (a human bronchial epithelial cell line) and THP‐1 cells (a human macrophage‐like cell line) were used as the in vitro models to investigate the underlying mechanism in this study. IL‐8 expression was increased in the cells treated with PM2.5 in a dose‐dependent manner. The water‐soluble and insoluble fractions of PM2.5 suspension were both shown to induce IL‐8 expression. PM2.5 exposure could obviously induce ROS (reactive oxygen species) generation, indicative of oxidative stress. Pretreatment with the antioxidant N ‐acetyl‐ l ‐cysteine (NAC) potently inhibited PM2.5‐induced IL‐8 expression. Employment of the transition metal chelators including TPEN ( N , N , N ', N '‐tetrakis (2‐pyridylmethyl) ethylenediamine) or DFO (desferrioxamine) inhibited IL‐8 expression induced by PM2.5 by over 20% in BEAS‐2B cells, but had minimal effect in THP‐1 cells. Pretreatment with the endocytosis inhibitor CytD markedly blocked IL‐8 expression induced by PM2.5 in both BEAS‐2B and THP‐1 cells. In summary, exposure to PM2.5 induced IL‐8 gene expression through oxidative stress induction and endocytosis in airway cells. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1869–1878, 2016.