Effects of sulfur dioxide on the expressions of MUC5AC and ICAM-1 in airway of asthmatic rats

Asthma is a chronic inflammatory disease characterized by infiltration and activation of various inflammatory cells and mucus secretion. To investigate the effects of SO2 on the expressions of asthma related-genes, male Wistar rats were challenged by ovalbumin (OVA) or SO2 (2 ppm) inhalation alone or together. Bronchoalveolar lavage and histopathologic examination were performed 24 h after the last treatment. The mRNA and protein levels of MUC5AC and ICAM-1 were analyzed in lungs and tracheas using real-time reverse transcription-polymerase chain reaction (real-time RT-PCR) assay, immunohistochemistry method and Western blot analysis, respectively. Exposure to OVA or to OVA plus inhaled SO2 significantly caused increases of the mRNA and protein levels of MUC5AC and ICAM-1 in lungs and tracheas of rats compared with the control (P < 0.05 or P < 0.01), but the increases of mRNA and protein levels after SO2 inhalation were not statistically significant. Exposure to OVA plus inhaled SO2 significantly not only induced the mRNA and protein expressions of these genes, but also induced the infiltration of inflammatory cells in lungs and tracheas and the increase of the numbers of inflammatory cells in bronchoalveolar lavage fluids (BALF), versus exposure to OVA alone. Meanwhile, a synergistic effect on the pathological changes between SO2 and OVA was observed in lungs after SO2 and OVA exposure. These results suggested that SO2 could increase the expressions of MUC5AC and ICAM-1 on the transcription and translation levels in the lungs and tracheas from asthmatic rats, which might be one of the possible mechanisms that SO2 pollution aggravates asthma disease.