Study Of The Immune Mechanism Of Lung Injury Incuded By Atmospheric PM2.5

Objective To observe the immune mechanism of lung injury incuded by atmospheric PM2.5.Methods:(1)To observe pathological changes under microscopy after HE staining.(2)The blood were collected by abdominal aorta to detect the levels of interleukin-6(IL-6)、IL-17a、TGF-β1 at 12 days after the setting up models. The BALF were collected to detect the total and differential cell counts. The pathological changes of lung were observed under microscopy after HE staining. The expression of TGF-β1, Smad2, RORγt and Foxp3 m RNA were detected by real-time PCR. And analysis of correlation between the m RNA levels of Smad2, RORγt, Foxp3 and the contents of IL-6, IL-17 a, TGF-β1 were performed. Results:(1)Pathologic changes of lung: No obvious pathological changes of pulmonary alveoli were showing in Ctrl and sham groups. The pulmonary alveoli wall of rats in L, M, H groups became thin and collapse with a great number of inflammatory cells infiltrated in the alveolar septum. Tissue injury aggravated dose-dependently.(2) The levels of IL-6, IL-17 a, TGF-β1 in serum were no significant difference among the Ctrl,sham and SB431542 groups(P>0.05). Compared with the Ctrl, sham and SB431542 groups, the levels of IL-6, IL-17 a, TGF-β1 in serum increased significantly in PM2.5group(P<0.05).(3) It showed no significant difference of cell counts of Lymphocyte,Eosinophil, Neutrophile and Macrophage(P>0.05) in BALF in Ctrl and sham groups.Compared with the sham group, the levels of Lymphocyte, Eosinophil, Neutrophile in PM2.5 group increased(P<0.05) while the cell count of Macrophage decresed(P<0.05).The levels of Lymphocyte, Eosinophil, Neutrophile in SB431542 group were lower than those in PM2.5 group. The levels of Macrophage increased in SB431542 group compared with the PM2.5 group(P<0.05).(4) Pathologic changes of lung: Standard size and integrated structure of pulmonary alveoli of rats were found in Ctrl and shamgroups.Obvious pathological damage of lung characterized with inflammatory cell infiltration,widen and fracture alveoli wall were showed in PM2.5 group. SB431542 group showed a lesser extent in pathological damage of lung.(5) The expression levels of Smad2, TGF-β1,RORγt and Foxp3 m RNA detected by real-time PCR: No significant difference in the expression of Smad2, TGF-β1, RORγt and Foxp3 m RNA were seen in the Ctrl, sham andSB431542 groups(P>0.05). Compared to the Ctrl, sham and SB431542 groups, the m RNA levels of Smad2, TGF-β1, RORγt and Foxp3 in PM2.5 group increased significantly(P<0.05).(6) Analysis of correlation between the m RNA levels of Smad2,RORγt, Foxp3 and the contents of IL-6, IL-17 a and TGF-β1 in serum: The Smad2 m RNA was positively correlated with the expression level of IL-6, IL-17 a and TGF-β1 in serum(the correlation coefficent: r=0.817, 0.826 and 0.862, P<0.05); The RORγt m RNA was positively correlated with the expression level of IL-6, IL-17 a and TGF-β1 in serum(the correlation coefficent:r=0.890, 0.823 and 0.818, P<0.05); The Foxp3 m RNA was positively correlated with the expression level of IL-6, IL-17 a and TGF-β1 in serum(the correlation coefficent: r=0.912, 0.812 and 0.846, P<0.05).Conclusion: Lung injury in rats can be induced by atmospheric PM2.5 in dose-dependent way. The underlying mechanism of lung injury induced by atmospheric PM2.5 may be the accumulating of proinflammatory cytokines of IL-6, IL-17 a and TGF-β1, which were the consequence of activating expression of Smad2, RORγt and Foxp3 resulted from the increased expression of TGF-β1.