title: [Effects of PM2.5 on phagocytic function of alveolar macrophages in chronic obstructive pulmonary disease mice].
abstract: OBJECTIVE
  To investigate the effects of fine particulate matter with a mean aerodynamic diameter ≤2.5 μm (PM2.5) collected from Lanzhou city on phagocytic function of alveolar macrophages (AM) in chronic obstructive pulmonary disease (COPD) mice.
  
  
  METHODS
  Forty male mice were randomly divided into four groups: healthy group, healthy PM2.5 group, COPD group and COPD PM2.5 group. COPD mice were established by cigarette smoking. PM2.5 (10 mg/kg) collected by air sampler was intratracheally instilled in healthy PM2.5 group and COPD PM2.5 group. Mice were sacrificed after 14 days, and alveolar macrophages (AM) were isolated. Mean fluorescence intensity (MFI) and the positive percent of alveolar macrophages engulfing flurescein isothiocyanate-labeled Escherichia coli (FITC-E.coli) (AM%) were detected by flow cytometry. Total antioxidative capacity (TAC) was measured by O-phenanthroline colorimetry. Malondialdehyde (MDA) was measured by thiobarbiturieacid colorimetry and myeloperoxidase (MPO) was measured by O-dianisidine colorimetry.
  
  
  RESULTS
  The peak inspiratory flow (PIF), peak expiratory flow (PEF) and dynamic compliance (Cdyn) of COPD group were significantly lower than healthy control group. The pathology of COPD group showed disruption of alveolar septa, formation of emphysema, and that the number of alveoli had a significant reduction. The MFI and AM% in COPD group were significant lower than healthy group (14.1±1.7 vs 43.2±6.1, 9.2%±2.3% vs 69.1%±8.3%)(all P<0.01). Comparing to healthy group and COPD group, the MFI and AM% in healthy PM2.5 group (20.3±4.5, 40.4%±4.4%) and COPD PM2.5 group (7.5±1.3, 6.0%±2.2%) were respectively lowered. The level of TAC in COPD group was significantly lower than healthy group [(3.10±0.64) vs (15.43±0.69)U/mg], the levels of MDA and MPO in COPD group were higher than healthy group[(2.72±0.13) vs (1.31±0.16) nmol/mg, (1.63±0.11) vs (0.92±0.13)U/g] (all P<0.01). In both healthy PM2.5 group and COPD PM2.5 group, the levels of TAC [(6.75±1.06), (2.34±0.61) U/mg] were lower than their corresponding control group; while the levels of MDA [(1.96±0.31), (3.20±0.19) nmol/mg] and the levels of MPO [(1.01±0.19), (1.74±0.13) U/g] were increased (all P<0.01). For the COPD group at baseline and after the intervention of PM2.5, the MFI and AM% showed positive correlation with the levels of TAC, and negative correlation with the levels of MDA , and negative correlation with the levels of MPO (all P<0.05). For health group at baseline and after the intervention PM2.5, the above relationships still existed (all P<0.05).
  
  
  CONCLUSIONS
  PM2.5 can damage phagocytosis of AM and exacerbate oxidative stress in COPD mice, and AM phagocytosis impairment by PM2.5 is closely associated with oxidative stress.
authors.affiliation: Department of Gerontal Respiratory Medicine, the First Hospital of Lanzhou University, Lanzhou 730000, China.
authors.forename: Juan
authors.initials: J
authors.lastname: Shu
authors.forename: Xiaoju
authors.initials: X
authors.lastname: Liu
authors.forename: Xu
authors.initials: X
authors.lastname: Chu
authors.forename: Jingman
authors.initials: J
authors.lastname: Qiu
authors.forename: Xiaoli
authors.initials: X
authors.lastname: Zeng
authors.forename: Hairong
authors.initials: H
authors.lastname: Bao
mesh_terms: D000818:Animals; D008168:Lung; D016676:Macrophages, Alveolar; D008297:Male; D008315:Malondialdehyde; D051379:Mice; D018384:Oxidative Stress; D052638:Particulate Matter; D010587:Phagocytosis; D011650:Pulmonary Alveoli; D029424:Pulmonary Disease, Chronic Obstructive; D011656:Pulmonary Emphysema; D012907:Smoking; D014026:Nicotiana
chemical_list: D052638:Particulate Matter; D008315:Malondialdehyde