Journal
TOXICOLOGY IN VITRO
Volume 70, Issue -, Pages -Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.tiv.2020.105040
Keywords
Toluene diisocyanate; Autophagy; Human bronchial epithelial cells; Inflammation; Airway remodeling
Categories
Funding
- Innovation Project of Shandong Academy of Medical Sciences
- Academic Promotion Programme of Shandong First Medical University [2019QL001]
- National Natural Science Foundation of China [81872603]
- Natural Science Foundation of Shandong Province [ZR2016YL015]
- Clinical Medicine Technology Innovation Plan of Jinan City [201907024]
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The study demonstrated that autophagy activation in 16HBE cells treated with TDI-HSA could enhance ROS release, Nrf2 expression, airway inflammation, and airway remodeling protein expression, while inhibiting autophagy could alleviate the inflammatory response and attenuate airway remodeling.
Toluene-diisocyanate (TDI) is one of the main causes of occupational asthma. To study the role of autophagy in TDI-induced airway inflammation and airway remodeling in bronchial airway epithelial (16HBE) cells. We treated 16HBE cells with TDI-human serum albumin (TDI-HSA) conjugate to observe reactive oxygen species (ROS) release, autophagy activation, airway inflammation and airway remodeling. 3-Methyladenine (3-MA) and Rapamycin (Rapa) intervention were used to explore the effects of autophagy on inflammatory response and protein expression related to airway remodeling in 16HBE cells treated with TDI-HSA. Experimental results suggested that various concentrations of TDI-HSA (0, 40, 80 and 120 mu g/mL) increased the release of ROS and the expression of Nrf2, activated autophagy and increased the expression of AMPK, Beclin-1, LC3 and decreased the expression of p62, promoted the levels of IL-5, IL-6 and IL-8 in 16HBE cells. Results also showed that E-cadherin expression decreased but an increase was observed in a-SMA and MMP-9 in the TDI-HSA group. The treatment of TDI-HSA combined with Rapa aggravated the above reaction whereas the inverse was true for TDI-HSA combined with 3-MA. These results indicated that autophagy is involved in TDI-induced airway inflammation and airway remodeling as a positive regulatory mechanism, inhibiting autophagy can significantly alleviate the TDI-induced inflammatory response and attenuate airway remodeling protein expression in 16HBE cells.
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