Histological changes in smoking and COPD mice with short-term exposure of PM2.5

Background: Epidemiological studies reported PM2.5 is associated with exacerbation of COPD, but the mechanism is unclear. And evidence about toxicity of PM2.5 on smokers is absence. Objective: To observe the short-term toxicity of PM2.5 to the smoking mice and the COPD mice. Method: Four groups were established: control, LPS as COPD positive control, PM2.5 and LPS+PM2.5. Normal saline, LPS, PM2.5 and a mixture of LPS and PM2.5 were respectively intra-tracheally administered to male C57BL/6J mice once a day on days 0, 7 and 14. The later three groups were exposured to cigarette smoke on days 1-6, 8-13 and 15-28. Sections of left lower lobes were subjected to hematoxylin and eosin (HE) staining. Mean linear intercept(MIL)was used to measure airspace enlargement. Result: Group LPS, PM2.5 and LPS+PM2.5 all showed marked hyperplasia and degeneration of bronchial epithelial cells and alveolar wall destruction with alveolar space enlargement. Secretions and hyperemia were seen in group PM2.5 and PM2.5+LPS, respectively[Figure 1(A)]. MLI had no difference among these three groups, which indicated they had similar degree of emphysema. MLI was significantly higher in the LPS group (p Conclude: Short-term exposure of PM2.5 can cause COPD-like changes in smoking mice, and acute inflammatory response in both smoking and COPD mice.