Effect of PM2.5 on airway inflammation in asthmatic mice

Objective To evaluate the effect of PM2.5 on airway inflammation in asthmatic mice, to verify the severe asthma airway inflammation induced by PM2.5. Methods ①BALB/c mice were randomly divided into four groups: the control group (NC group), the asthma group (AC group), the asthma+ low dose PM2.5 group (AP-L group), the asthma+ high PM2.5 group (AP-H group). ②Mice in the last three groups were sensitized and challenged by OVA.Mice in the two PM2.5 group were given 100 μl PM2.5 suspension.③Airway responsiveness to acetylcholine chloride (Ach) was measured in mice 24 h after the last challenge.Bronchoalveolar lavage fluid (BALF) was centrifuged and total cell and neutrophil cell were counted, enzyme linked immunosorbent assay were used to determine IL-17 levels in BALF and serum.The airway inflammatory infiltration was detected by haematoxylin and eosin (HE) staining. Results ①An OVA-induced mouse models with acute asthma were successfully established.②No significant difference was found in baseline airway resistance among the four groups.At dose of Ach from 10 to 270 μg.kg-1 the airway resistance in the AC, AP two groups was obvious increased compared with the NC group, the AP two groups had significant greater airway resistant than AC group in a dose-dependent manner (P<0.05). Very few inflammatory cells were detected in NC mice, a significant increase in total and neutrophil cell number was exhibited in AC and AP animals, the AP two groups had greater increase compared with AC group in a dose-dependent manner (P<0.05). Levels of IL-17 in BALF and serum were significantly increased in AC and AP groups than NC group, the AP two groups had greater increase compared with AC group in a dose-dependent manner (P<0.05). In the following hematoxylin and eosin, the structure of lung tissue in NC group is normal, the inflammation of air flue in AP-H group is obvious, while airway inflammation in AC and AP-L group attenuated. Conclusions Magnetic exposure to PM2.5 may aggravate the airway inflammation and airway hyperresponsiveness in asthmatic mice and form severe asthma. Key words: PM2.5; Severe asthma; Neutrophil airway inflammation; Interleukin-17