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Updated: Jul 4, 2026
Alveolar Macrophage Phagocytosis and Bacteria Clearance in Mice
Published on: March 2, 2019
Macrophage dysfunction and susceptibility to pulmonary Pseudomonas aeruginosa infection in surfactant protein
Stephan W Glasser1, Albert P Senft, Jeffrey A Whitsett
1Division of Pulmonary Biology, Department of Pediatrics, Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45229-3039, USA. steve.glasser@cchmc.org
Abstract:
To determine the role of surfactant protein C (SP-C) in host defense, SP-C-deficient (Sftpc-/-) mice were infected with the pulmonary pathogen Pseudomonas aeruginosa by intratracheal injection. Survival of young, postnatal day 14 Sftpc-/- mice was decreased in comparison to Sftpc+/+ mice. The sensitivity to Pseudomonas bacteria was specific to the 129S6 strain of Sftpc-/- mice, a strain that spontaneously develops interstitial lung disease-like lung pathology with age. Pulmonary bacterial load and leukocyte infiltration were increased in the lungs of Sftpc-/- mice 24 h after infection. Early influx of polymorphonuclear leukocytes in the lungs of uninfected newborn Sftpc-/- mice relative to Sftpc+/+ mice indicate that the lack of SP-C promotes proinflammatory responses in the lung. Mucin expression, as indicated by Alcian blue staining, was increased in the airways of Sftpc-/- mice following infection. Phagocytic activity of alveolar macrophages from Sftpc-/- mice was reduced. The uptake of fluorescent beads in vitro and the number of bacteria phagocytosed by alveolar macrophages in vivo was decreased in the Sftpc-/- mice. Alveolar macrophages from Sftpc-/- mice expressed markers of alternative activation that are associated with diminished pathogen response and advancing pulmonary fibrosis. These findings implicate SP-C as a modifier of alveolar homeostasis. SP-C plays an important role in innate host defense of the lung, enhancing macrophage-mediated Pseudomonas phagocytosis, clearance and limiting pulmonary inflammatory responses.
Insights
Surfactant protein C (SP-C) deficiency impairs lung host defense against Pseudomonas aeruginosa by reducing macrophage phagocytosis and increasing inflammation. SP-C is crucial for maintaining lung homeostasis and fighting bacterial infections.
Area of Science:
- Pulmonary immunology
- Innate immunity
- Host-pathogen interactions
Background:
- Surfactant protein C (SP-C) is vital for lung function.
- Its role in host defense against bacterial pathogens is not fully understood.
- SP-C deficient mice (Sftpc-/-) on a specific genetic background develop lung pathology.
Purpose of the Study:
- To investigate the role of SP-C in host defense against Pseudomonas aeruginosa infection.
- To determine how SP-C deficiency affects lung inflammation and bacterial clearance.
Main Methods:
- Intratracheal instillation of Pseudomonas aeruginosa into Sftpc-/- and wild-type (Sftpc+/+) mice.
- Assessment of survival, bacterial load, leukocyte infiltration, mucin expression, and alveolar macrophage phagocytic activity.
- Analysis of macrophage activation markers.
Main Results:
- Sftpc-/- mice exhibited decreased survival and increased pulmonary bacterial load post-infection.
- SP-C deficiency led to enhanced pulmonary inflammation, including increased leukocyte infiltration and mucin expression.
- Alveolar macrophages from Sftpc-/- mice showed reduced phagocytic capacity and expressed markers of alternative activation.
Conclusions:
- SP-C is essential for effective innate host defense in the lungs.
- SP-C enhances Pseudomonas phagocytosis and clearance by alveolar macrophages.
- SP-C plays a critical role in limiting pulmonary inflammatory responses and maintaining alveolar homeostasis.
