[Effects of diesel exhaust particles inhalation on immediate reaction in asthma rats].

OBJECTIVE: The role of air pollution on asthma can not be ignored, diesel exhaust particles (DEP) in the air is one of the most important pollutants. This study aimed to investigate the effect and mechanism of DEP inhaled on immediate reaction in the asthma rats. METHOD: Sixty male Wistar rats of "Clean" grade, 6 - 7 week-old, with an average weight of (140 +/- 20) g were used in this study. The rats were randomly divided into 6 groups, 10 in each. Group A was treated with normal saline attack as a negative control, Group B with ovalbumin attack as a positive control. After ovalbumin attack, groups C, D, E, F continued to inhale DEP for 1 week, 2 weeks, 3 weeks and 4 weeks, respectively. The concentration of DEP was 200 microg/ml, the animals were subjected to inhalation of ultrasound nebulized DEP for 30 min per day. One week after all the attacks were concluded, Group A was stimulated with normal saline for 30 min, other groups were stimulated with ovalbumin. Then the airway resistance was determined with multi-channel signal acquisition and processing system and compared. The changes in neutrophils, eosinophils, and other inflammatory cells of BALF and the pathological changes in lung tissue, including epithelial cells loss, the inflammatory cells infiltration around the airway, basement membrane fibrosis, goblet cell hyperplasia etc. were observed. The concentration of IL-5 and gamma-interferon in the lung tissues, and the changes of serum IgE etc. were determined. RESULT: Airway resistance values of group A, B, C, D, E, F after ovalbumin excitation for 30 min were (3.56 +/- 0.21), (7.06 +/- 0.63), (6.46 +/- 0.38), (7.47 +/- 0.33), (8.87 +/- 0.61), (11.00 +/- 0.69) cm H2O/(ml.s). No airway hyperresponsiveness occurred in group A, while Groups B, C, D, E, F had higher airway resistance than group A, group E and F had higher airway resistance than that of group B, the differences were statistically significant. And the airway resistance was different in each group among 0 min, 10 min, 20 min and 30 min (F = 160.646, 148.901, 162.204, 156.186, P < 0.01 for both). The time of DEP inhalation and the airway resistance was positively correlated (r = 0.948, P < 0.01); IgE concentrations of the serum between groups B, C, D, E, F was not significantly different (P > 0.05), but higher than that of group A (F = 2.639, P < 0.01). The infiltrated inflammatory cells included eosinophils and lymphocytes, etc. The percentages of neutrophil(%) were (4.3 +/- 2.0), (9.7 +/- 5.2), (10.3 +/- 5.6), (13.0 +/- 5.2), (42.6 +/- 18.3), (55.3 +/- 6.9). The groups E and F had higher percentage than Group A and Group B (F = 114.226, P < 0.01). The percentages of eosinophils(%) were 0, (11.9 +/- 3.8), (15.8 +/- 6.3), (13.0 +/- 4.9), (21.1 +/- 5.6), (27.1 +/- 4.8). The difference between Groups B, C, D, E, F and Group A was statistically significant. There was significant difference between groups C, D, E, F and group B (F = 46.462, P < 0.05); Lung tissue biopsy in group A showed that the epithelial cells were intact, no inflammatory cells infiltrations were found around the airways, instead, mainly ciliated columnar epithelial cells and only a small number of goblet cells were seen without basement membrane fibrosis. With the inhalation of DEP, the epithelial cells showed gradual necrosis, disruption and loss, goblet cells showed hyperplasia, and infiltrations with inflammatory cells were seen around the airway. In the lung tissue, concentrations of IL-5 in group B, C, and E were (12.8 +/- 2.8), (17.1 +/- 5.2), (18.6 +/- 4.2) pg/mg, the difference between groups C, E and group B was statistically significant (F = 4.236, P < 0.01), the difference in gamma-interferon concentration among all groups was not statistically significance (F = 1.185, P > 0.05). CONCLUSION: DEP inhalation increased the airway responsiveness of asthma rats in immediate reaction, promoted the lung epithelial cell loss, inflammatory cell infiltration, basement membrane fibrosis and goblet cell hyperplasia.