Cigarette dust particles induced lung function injury of chronic obstructive pulmonary disease in mice

AIM: To investigate the pathogenesis of chronic obstructive disease (COPD) in mice by using nasal drip of cigarette dust particles (DSP) induced pulmonary function damage model.METHODS: BALB/c mice were randomly divided into control group, LPS 100 mg/L group, DSP 0.75 mL/L group, DSP 1.5 mL/L group and DSP 3 mL/L group for 30 days. The method of nasal drip was used for 30 days to establish the COPD model. Rrs, Ers, Crs, Est, Cst, P-3/8Rn, P-3/8G and P-3/8H were measured for evaluating lung function of the mice in each group by the method of FlexiVent. The effect on the increase of airway resistance induced by methacholine (Mach) was determined using main bronchial rings by Myograph method. The HE, Masson and Resorcinol fuchsin staining of mouse tracheas and lung tissues were conducted. RESULTS: Continuous nasal drip with DSP for 30 days increased Rrs, Ers, Est, P-3/8Rn and decreased Crs, Cst, P-3/8G and P-3/8H in the mice. DSP significantly shifted the dose-effect curve of tracheal contraction induced by Mach to the left, increased the sensitivity of the airway to Mach, and significantly increased the maximal contractile airway effect of Mach. Exposure to DSP caused fibrosis of airway subepithelial, deposition of collagen in the airway basement membrane under the reticular plate, induced reticular plate thickening, pulmonary bronchial lumen serious deformation, and the inflammatory cell infiltration in the lung of mice. Significantly increased alveolar wall muscle fibers and collagen fibers were also observed. CONCLUSION: The lung function and pathomorphological changes of COPD mice induced by 30 days nasal drip of cigarette dust particles were similar to those of human COPD.