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Published on: November 27, 2014
Phagocytosis of unopsonized Pseudomonas aeruginosa by murine macrophages is a two-step process requiring glucose
1Department of Pediatrics, University of British Columbia, Vancouver, Canada.
Abstract:
Pseudomonas aeruginosa is an important pulmonary pathogen in cystic fibrosis, but the means by which it evades host defenses is understood poorly. Macrophages (M phi) are critical in protecting the lung and mucosal surfaces against infection and may need to perform their functions in the absence of opsonins before the evolution of an inflammatory response. The purpose of the present study was to define factors that regulate the capacity of macrophages to mediate nonopsonic phagocytosis. Phagocytosis of unopsonized P. aeruginosa by murine peritoneal and pulmonary alveolar M phi s was absolutely dependent upon the presence of glucose; only D-mannose could substitute. Glucose-dependent phagocytosis appears to be selective for P. aeruginosa by M phi s; ingestion of unopsonized zymosan, opsonized P. aeruginosa, EIgG, and E (IgM)C occurred in the presence or absence of glucose as did-ingestion of unopsonized P. aeruginosa by polymorphonuclear leukocytes. M phi binding and phagocytosis of unopsonized P. aeruginosa appeared to occur by a mechanism independent of complement receptor 3 and mannose receptors. Phagocytosis of P. aeruginosa killed by tobramycin or Formalin was glucose dependent, suggesting that the glucose exerted its effects on the M phi rather than the bacteria. The predilection of P. aeruginosa for lower airway disease in patients with cystic fibrosis might be explained in part by the unique dependency upon glucose for M phi phagocytosis.
Insights
Glucose is essential for macrophages to engulf Pseudomonas aeruginosa, a key pathogen in cystic fibrosis lung infections. This discovery sheds light on how bacteria evade immune responses in the lungs.
Area of Science:
- Immunology
- Microbiology
- Pulmonary Medicine
Background:
- Pseudomonas aeruginosa is a significant lung pathogen, particularly in cystic fibrosis patients.
- Macrophages are crucial for lung defense, especially in the early, non-opsonic stages of infection.
- Mechanisms of how macrophages phagocytose unopsonized P. aeruginosa are poorly understood.
Purpose of the Study:
- To identify factors regulating macrophage-mediated non-opsonic phagocytosis.
- To investigate the role of glucose in the phagocytosis of P. aeruginosa by macrophages.
Main Methods:
- Murine peritoneal and pulmonary alveolar macrophages were used.
- Phagocytosis assays were performed with unopsonized P. aeruginosa in the presence or absence of glucose and other sugars.
- Binding and phagocytosis were assessed using various bacterial preparations and immune cells.
Main Results:
- Macrophage phagocytosis of unopsonized P. aeruginosa was strictly dependent on glucose; D-mannose served as a substitute.
- This glucose dependency was specific to P. aeruginosa, as other particles (zymosan, opsonized bacteria, antibody-coated cells) were ingested regardless of glucose.
- The mechanism was independent of complement receptor 3 and mannose receptors on macrophages.
- Glucose influenced the macrophages, not the bacteria, as heat-killed or formalin-killed P. aeruginosa also required glucose for phagocytosis.
Conclusions:
- Glucose is a critical factor enabling macrophages to phagocytose unopsonized Pseudomonas aeruginosa.
- This glucose-dependent mechanism may explain the preferential colonization of the lower airways by P. aeruginosa in cystic fibrosis patients.
- Understanding this interaction could lead to novel therapeutic strategies for P. aeruginosa lung infections.
