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Updated: Dec 29, 2025
Alveolar Macrophage Phagocytosis and Bacteria Clearance in Mice
Published on: March 2, 2019
Decreased expression of a phagocytic receptor Siglec-1 on alveolar macrophages in chronic obstructive pulmonary
Atsushi Tanno, Naoya Fujino1, Mitsuhiro Yamada2
1Department of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryocho, Aobaku, Sendai, 980 8574, Japan. nfujino@med.tohoku.ac.jp.
Background:
Alveolar macrophages are professional phagocytes that remove microbial pathogens inhaled into the lung. The phagocytic ability is compromised in chronic obstructive pulmonary disease (COPD). However, the molecular mechanisms underlying this defect in phagocytosis are not clearly defined.
Materials And Methods:
Cell suspensions were collected from lung tissues of patients undergoing lung resection. Alveolar macrophages were detected as FSChi/ SSChi/CD45+/CD206+ cells in the isolated cell suspension by flow-cytometry. The cell surface expression of plasma membrane-bound phagocytic receptors (Fcγ receptor I (FcγRI), a complement receptor CD11b, macrophage scavenger receptor-1 (MSR-1), CD36 and Siglec-1) was determined on the alveolar macrophages. Correlations between the expression levels of the phagocytic receptors and disease severity were analysed. Phagocytosis of fluorescence-tagged bacteria by human alveolar macrophages was evaluated.
Results:
The flow-cytometry analyses revealed that FcγRI, CD11b, MSR-1 and Siglec-1, but not CD36, were expressed on human alveolar macrophages. Among these receptors, Siglec-1 expression was significantly decreased on alveolar macrophages in COPD ex-smokers (n = 11), compared to control never-smokers (n = 11) or control ex-smokers (n = 9). The Siglec-1 expression on alveolar macrophages was significantly correlated with lung function (forced expiratory volume in 1 s) and with the severity of emphysema. Treatment of human alveolar macrophages with an anti-Siglec1 blocking antibody decreased phagocytosis of non-typeable Haemophilus influenzae (NTHi).
Conclusion:
Our findings demonstrated reduced expression of Siglec-1 on alveolar macrophages in COPD, which is involved in engulfment of NTHi.
Insights
Siglec-1 expression is reduced on alveolar macrophages in chronic obstructive pulmonary disease (COPD) patients. This decrease in Siglec-1 impacts the engulfment of bacteria, suggesting a novel mechanism in COPD pathogenesis.
Area of Science:
- Pulmonary immunology
- Cellular and molecular mechanisms of lung disease
Background:
- Alveolar macrophages are crucial for lung defense against inhaled pathogens.
- Phagocytic dysfunction in alveolar macrophages is a hallmark of chronic obstructive pulmonary disease (COPD).
- The molecular underpinnings of impaired phagocytosis in COPD remain incompletely understood.
Purpose of the Study:
- To investigate the expression of phagocytic receptors on alveolar macrophages in COPD patients.
- To determine the correlation between receptor expression, disease severity, and phagocytic capacity.
- To elucidate the role of Siglec-1 in alveolar macrophage phagocytosis of bacteria.
Main Methods:
- Alveolar macrophages were isolated from lung tissues of COPD patients and controls.
- Flow cytometry was used to quantify cell surface expression of phagocytic receptors, including Siglec-1.
- Phagocytosis assays evaluated bacterial engulfment by alveolar macrophages, with and without Siglec-1 blockade.
Main Results:
- Siglec-1, FcγRI, CD11b, and MSR-1 were expressed on human alveolar macrophages.
- Siglec-1 expression was significantly reduced in COPD ex-smokers compared to controls.
- Reduced Siglec-1 expression correlated with decreased lung function and emphysema severity, impairing bacterial phagocytosis.
Conclusions:
- COPD is characterized by reduced Siglec-1 expression on alveolar macrophages.
- Siglec-1 plays a significant role in the phagocytosis of non-typeable Haemophilus influenzae (NTHi) by alveolar macrophages.
- Targeting Siglec-1 may offer a therapeutic strategy for improving lung defense in COPD.
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