Related Experiment Video
Updated: Mar 10, 2026

Quantification of Efferocytosis by Single-cell Fluorescence Microscopy
Published on: August 18, 2018
Elimination of Pseudomonas aeruginosa through Efferocytosis upon Binding to Apoptotic Cells
Darío Capasso1, María Victoria Pepe1, Jéssica Rossello2
1Instituto de Investigaciones Biotecnológicas Dr. Rodolfo A. Ugalde (IIB-INTECH), Universidad Nacional de San Martín, Consejo Nacional de Investigaciones Científicas y Técnicas (UNSAM-CONICET), San Martín, Buenos Aires, Argentina.
Abstract:
For opportunistic pathogens such as Pseudomonas aeruginosa, the mucosal barrier represents a formidable challenge. Infections develop only in patients with altered epithelial barriers. Here, we showed that P. aeruginosa interacts with a polarized epithelium, adhering almost exclusively at sites of multi-cellular junctions. In these sites, numerous bacteria attach to an extruded apoptotic cell or apoptotic body. This dead cell tropism is independent of the type of cell death, as P. aeruginosa also binds to necrotic cells. We further showed that P. aeruginosa is internalized through efferocytosis, a process in which surrounding epithelial cells engulf and dispose of extruded apoptotic cells. Intracellularly, along with apoptotic cell debris, P. aeruginosa inhabits an efferocytic phagosome that acquires lysosomal features, and is finally killed. We propose that elimination of P. aeruginosa through efferocytosis is part of a host defense mechanism. Our findings could be relevant for the study of cystic fibrosis, which is characterized by an exacerbated number of apoptotic cells and ineffective efferocytosis.
Insights
Pseudomonas aeruginosa adheres to dead epithelial cells at junctions and is engulfed via efferocytosis. This process eliminates the bacteria, suggesting a host defense mechanism relevant to cystic fibrosis.
Area of Science:
- Microbiology and Immunology
- Cell Biology
- Pathogen-Host Interactions
Background:
- Mucosal barriers are critical defenses against opportunistic pathogens like Pseudomonas aeruginosa.
- P. aeruginosa infections typically occur in individuals with compromised epithelial barriers.
Purpose of the Study:
- To investigate the interaction of P. aeruginosa with polarized epithelial cells.
- To elucidate the mechanisms of P. aeruginosa entry and intracellular fate within epithelial cells.
- To explore the role of efferocytosis in controlling P. aeruginosa infection.
Main Methods:
- Microscopy-based analysis of P. aeruginosa interaction with polarized epithelial cell monolayers.
- Investigation of bacterial adherence to apoptotic and necrotic cells.
- Characterization of bacterial internalization via efferocytosis and intracellular trafficking.
Main Results:
- P. aeruginosa preferentially adheres to extruded apoptotic cells at multicellular junctions.
- Bacterial tropism for dead cells is independent of the cell death type (apoptotic or necrotic).
- P. aeruginosa is internalized through efferocytosis and resides within phagosomes that acquire lysosomal features, leading to bacterial killing.
Conclusions:
- Efferocytosis serves as a host defense mechanism to eliminate P. aeruginosa.
- This pathway is crucial for clearing bacteria associated with dead or dying epithelial cells.
- Findings may inform strategies for treating infections in conditions like cystic fibrosis, marked by excessive cell death and impaired efferocytosis.
More Related Videos
Related Concept Videos
Phagocytosis of Apoptotic Cells
Normal cells contain receptors that prevent them from being recognized...
The Extrinsic Apoptotic Pathway
Apoptosis
Overview of Cell Death
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
The Intrinsic Apoptotic Pathway
Autophagic Cell Death
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...

