Journal
JOURNAL OF HAZARDOUS MATERIALS
Volume 385, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.jhazmat.2019.121566
Keywords
PM2.5; Post-exposure toxicity; Pulmonary fibrosis; Chronic inflammation; Epithelial mesenchymal transition
Categories
Funding
- National Key R&D Program of China [2017YFC0211600, 2017YFC0211602, 2017YFC0211606]
- National Natural Science Foundation of China [81571130090, 81673204, 81930091]
- Support Project of High-level Teachers in Beijing Municipal Universities in the Period of 13th Five-year Plan [CIT TCD201804089]
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Up to now, while some toxicological studies have identified pulmonary fibrosis immediately induced by long-term PM2.5 exposure, there has been no evidence indicating, whether short-term exposure can lead to post-exposure development of pulmonary fibrosis. Here, we treated rats with PM(2.5 )for 1 month (10 times), followed by normal feeding for 18 months. F-18-FDG intake, which is linked with the initiation and development of pulmonary fibrosis in living bodies, was found to gradually increase in lung following exposure through micro PET/CT imaging. Histolopathological examination revealed continuous deterioration of pulmonary injury post-exposure. Collagen deposition and hydroxyproline content continued to increase all along in the post-exposure duration, indicating pulmonary fibrosis development. Chronic and persistent induction of pulmonary inflammatory gene expression (Tnf, Il1b, Il6, Ccl2, and Icam1), epithelial mesenchymal transition (EMT, reduction of E-cadherin and elevation of fibronectin) and RelA/p65 upregulation, as well as serum inflammatory cytokine production, were also found in PM2.5-treated rats. Pulmonary oxidative stress, manifested by increase of MDA and decrease of GSH and SOD, was induced during exposure but disappeared in later post-exposure duration. These results suggested that short-term PM2.5 exposure could lead to sustained post-exposure pulmonary fibrosis development, which was mediated by oxidative-stress-initiated NF-kappa B/inflammation/EMT pathway.
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