<![CDATA[Objective: Pulmonary fibrosis in asthma is marked by a rapid decline in lung function. Unfortunately, the environmental factors aggravating this condition are still poorly understood. To date, the pathomechanism of exposure to coal dust affecting the subepithelial fibrosis in asthma remains unclear. Methods: Twenty-fourth female BALB/C mice were divided into four group. The first group was control, the second was mice exposed to coal dust particulate matter (PM) (days 46-75), the third was OVA sensitized mice (Initial sensitization on day 0 and 14, re-sensitization days 21-75), and the fourth was made of OVA-sensitized mice and exposed coal dust PM. Results: The results showed coal dust PM significantly decreased levels of IL-13 BAL (p-value=0.001) but significantly elevated H2O2 BAL levels (p-value=0.001) and increased sub-epithelial bronchial fibrosis thickness (p-value= 0.000). This was based on the scale of fibrosis (0=<5 μm, 1=5-10 μm; 2=11-15 μm; 3=>15 μm; score 0-1=mild; 1-2=moderate; and 3= severe). The combination of ovalbumin sensitization and PM coal dust caused severe fibrosis (score 3).There was no significant association between IL-13, TGF-β3, H2O2, and MDA BAL with sub-epithelial fibrosis thickness. Conclusions: PM exposure to coal dust may increase sub-epithelial fibrosis of the bronchioles by a mechanism independent of inflammation and oxidative stress.Objective:Pulmonary fibrosis in asthma is marked by a rapid decline in lung function. Unfortunately, the environmental factors aggravating this condition are still poorly understood. To date, the pathomechanism of exposure to coal dust affecting the subepithelial fibrosis in asthma remains unclear. Methods: Twenty-fourth female BALB/C micewere divided into four group. The first group was control, the second was mice exposed to coal dust particulate matter (PM) (days 46-75), the third was OVA sensitized mice (Initial sensitization on day 0 and 14, re-sensitization days 21-75), and the fourth was made of OVA-sensitized mice and exposed coal dust PM. Results: The results showed coal dust PM significantly decreased levels of IL-13 BAL (p-value=0.001) but significantly elevated H2O2 BAL levels (p-value=0.001) and increased sub-epithelial bronchial fibrosis thickness (p-value=0.000). This was based on the scale of fibrosis (0=<5μm, 1=5-10μm; 2=11-15μm; 3=>15μm; score 0-1=mild; 1-2=moderate; and 3= severe). The combination of ovalbumin sensitization and PM coal dust caused severe fibrosis (score 3).There was no significant association between IL-13, TGF-β3, H2O2, and MDA BAL with sub-epithelial fibrosis thickness.Conclusions: PM exposure to coal dust may increase sub-epithelial fibrosis of the bronchioles by a mechanism independent of inflammation and oxidative stress.]]>
