Effect And Mechanism Of PM2.5 On Phagocytosis Of Alveolar Macrophage In COPD Mice

Objective To investigate the effects of PM2.5 in Lanzhou area on the alveolar macrophages phagocytic function and oxidative damage of COPD mice.Methods 40 male mice were randomly divided into healthy control group,healthy PM2.5 intervened group,COPD control group,COPD PM2.5 intervened group.COPD mice were exposed to cigarette smoke in 90 days,their lung function and pathological changes were observed.The mice of healthy and COPD PM2.5 intervened group were intratracheally injected with 10mg/kg PM2.5,were sacrificed after 14 days,isolated alveolar macrophages(AM),use flow cytometry method to detect the function of alveolar macrophages engulfed FITC-E.coli;use colorimetric method to measure the content of TAC,MDA,GSH and MPO in lung tissue.The aging curve of AM function and lung oxidative damage after PM2.5 intervention choose 1d,3d,7d,14d for the observation nodes.Results (1).After smoke exposure,the pulmonary function of COPD group were significantly lower than healthy control group,including the PIF(Peak inspiratory flow), PEF(Peak expiratory flow)、and Cdyn(Dynamic compliance),the difference was statistically significant(P<0.01).The pathology of COPD group alveolar wall is thinned,expanded and fractured,part of alveolar space emphysema is fused into bullae rupture,the number of alveoli has a significant reduced, no such change in healthy control group.The average lined interval (MLI) in COPD group were higher than healthy control group.(2).Time effect of PM2.5 on AM phagocytosis:After PM2.5 intervened healthy and COPD group,the function of AM in 1d,3d,7d,14d were lower than their control group.(3)The compare of AM phagocytosis in each group:The AM phagocytic percentage of positive cells and mean fluorescence intensity in COPD control group was (9.24±2.50)% and (14.89±1.43),significantly lower than the healthy control group (69.14±8.34)% and (41.47±5.89);after PM2.5 intervened,healthy PM2.5 intervention group,COPD PM2.5 intervention group the AM phagocytic percentage of positive cells and mean fluorescence intensity were (40.3±4.41)%,(17.76±5.27)and (7.43±1.87)%,(7.46±1.29),respectively lower than healthy control and COPD control group,the difference was statistically significant(P<0.01).(4)Time effect of PM2.5 on lung tissue oxidative injury:After PM2.5 intervened healthy and COPD group ld,3d,7d,14d,the level of lung tissue TAC,GSH were lower than its control group, MDA was higher than its control group;the content of MPO in healthy group 1d,7d was lower than control group,the difference was statistically significant(P<0.01),3d,14d had no significant difference than control group,COPD group 1d,14d group had no significant difference than COPD control group (P> 0.05).(5) Comparison of oxidative damage indicators in each group:after PM2.5 intervened,healthy PM2.5 intervention group and COPD PM2.5 intervention group their content of TAC,GSH was lower than healthy control and COPD control group,MDA was higher than control group,the level of MPO in COPD PM2.5 group was lower than COPD control group,the difference was statistically significant(P<0.01). (6).The correlation between the phagocytic function and the oxidative stress:Healthy group under basal state and after PM2.5 intervened,the AM phagocytic percentage of positive cells were positively correlated with the level of TAC(r respectively r= 0.746,0.771, P< 0.01～0.05), and MDA negative correlation(r respectively r=-0.843,-0.846,P<0.01),were positively correlated with GSH (r respectively r=0.761,0.793, P<0.01～0.05), was negatively correlated with MPO (r respectively r=-0.668,-0.869, P<0.01～0.05).COPD group under basal state and after PM2.5 intervened,the AM phagocytic percentage of positive cells were positively correlated with the level of TAC(r respectively=0.84,0.711,P<0.01～0.05), and MDA negative correlation (r respectively=-0.809,-0.818,P<0.01), were positively correlated with GSH (r respectively= 0.702,0.849,P<0.01), was negatively correlated with MPO (r respectively=-0.704,-0.701, P<0.01).Conclusion The AM phagocytosis function of COPD mice was lower than healthy control mice.After PM2.5 exposure,can damage healthy and COPD mice AM function, cause their lung tissue oxidative damage;PM2.5 to reduce AM phagocytic capacity can closely associated with oxidative stress.