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  • Title: Effects of SO2 derivatives on expressions of MUC5AC and IL-13 in human bronchial epithelial cells.
    Author: Li R, Meng Z.
    Journal: Arch Toxicol; 2007 Dec; 81(12):867-74. PubMed ID: 17520240.
    Abstract:
    Sulfur dioxide (SO2) is a common air pollutant, and inhaled SO2 in airway epithelium easily forms its soluble derivatives in vivo (bisulfite and sulfite), which are toxic to the respiratory system and related to the exacerbation of asthma. To investigate the effects of SO2 derivatives on the expressions of asthma related genes (MUC5AC and IL-13), the mRNA and protein levels of the two genes in cultured human bronchial epithelial (BEP2D) cells were analyzed using real-time reverse transcription-polymerase chain reaction (real-time RT-PCR) assay, immunocytochemistry method and enzyme-linked immunosorbent assay (ELISA), respectively. The results showed that the mRNA expressions of MUC5AC and IL-13 were significantly increased at different concentrations of SO2 derivatives (0.0001, 0.001, 0.01, 0.1 and 1.0 mM), and the maximum appeared at 0.01 mM for MUC5AC (3.9-fold) or at 0.001 mM for IL-13 (4.7-fold). Meanwhile, SO2 derivatives significantly increased the mRNA levels at 0, 0.5, 1, 4 and 24 h post-exposure with the maximum at 4 h post-exposure (25-fold for MUC5AC and 41-fold for IL-13). Furthermore, the protein levels of MUC5AC and IL-13 in BEP2D cells were significantly increased at different concentrations and different time courses exposed to SO2 derivatives, along with the maximum at 4 h post-exposure. These results lead to a conclusion that SO2 derivatives can increase the expressions of MUC5AC and IL-13 genes on the transcription and translation levels, and it suggests that SO2 derivatives can induce mucus over-production and inflammation responses in human bronchial epithelial cells and may have relations with asthma diseases. This might be one of the possible mechanisms that SO2 aggravates asthma disease.
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