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Updated: Mar 25, 2026
Alveolar Macrophage Phagocytosis and Bacteria Clearance in Mice
Published on: March 2, 2019
[Effects of PM2.5 on phagocytic function of alveolar macrophages in chronic obstructive pulmonary disease mice]
1Department of Gerontal Respiratory Medicine, the First Hospital of Lanzhou University, Lanzhou 730000, China.
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).
Conclusion:
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.
Insights
Fine particulate matter (PM2.5) impairs alveolar macrophage phagocytosis in mice with chronic obstructive pulmonary disease (COPD), worsening oxidative stress. This PM2.5-induced impairment is linked to increased oxidative stress markers.
Area of Science:
- Environmental Health
- Pulmonary Medicine
- Immunology
Background:
- Chronic obstructive pulmonary disease (COPD) is a major global health concern.
- Air pollution, particularly fine particulate matter (PM2.5), is a known exacerbating factor for respiratory diseases.
- Alveolar macrophages (AM) play a crucial role in lung defense and are susceptible to environmental insults.
Purpose of the Study:
- To investigate the impact of Lanzhou city-collected PM2.5 on the phagocytic function of alveolar macrophages (AM) in a mouse model of COPD.
- To assess the relationship between PM2.5 exposure, AM phagocytosis, and oxidative stress markers in healthy and COPD mice.
Main Methods:
- COPD was induced in mice via cigarette smoking.
- Mice were exposed to PM2.5 (10 mg/kg) intratracheally.
- Alveolar macrophages were isolated and their phagocytic capacity was measured using flow cytometry (MFI and AM%).
- Oxidative stress markers including total antioxidative capacity (TAC), malondialdehyde (MDA), and myeloperoxidase (MPO) were quantified.
Main Results:
- COPD mice exhibited reduced lung function and emphysematous changes.
- PM2.5 exposure significantly decreased AM phagocytic function (MFI and AM%) in both healthy and COPD mice.
- PM2.5 exposure increased oxidative stress markers (MDA, MPO) and decreased antioxidative capacity (TAC) in both groups.
- Impaired AM phagocytosis was positively correlated with TAC and negatively correlated with MDA and MPO levels.
Conclusions:
- PM2.5 exposure damages AM phagocytic function in COPD mice.
- PM2.5 exacerbates oxidative stress in COPD mice.
- Impairment of AM phagocytosis by PM2.5 is closely associated with increased oxidative stress.
