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Automated, High-Throughput Detection of Bacterial Adherence to Host Cells
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AlphaVBeta5 integrins mediates Pseudomonas fluorescens interaction with A549 cells
Elisabetta Buommino1, Marina Di Domenico2, Iole Paoletti1
1Department of Experimental Medicine, Section of Microbiology and Clinical Microbiology, Second University of Naples, Italy.
Frontiers in Bioscience (Landmark Edition)
|January 7, 2014
Summary
Pseudomonas fluorescens AF181 uses Alpha(v)Beta5 integrins and vitronectin to adhere to and invade human respiratory cells. Inhibiting these interactions reduces bacterial entry, offering potential therapeutic targets for P. fluorescens infections.
Area of Science:
- Microbiology
- Cell Biology
- Immunology
Background:
- Bacterial interaction with host cells is crucial for infection.
- Microbial binding to extracellular matrix proteins like vitronectin and integrins stimulates bacterial invasion.
- Pseudomonas fluorescens AF181, a clinically isolated strain, adheres to human respiratory epithelial cells and influences inflammation.
Purpose of the Study:
- To investigate the role of Alpha(v)Beta5 integrins and vitronectin in P. fluorescens AF181 adherence and invasion.
- To explore the involvement of host cell cytoskeleton and tyrosine kinases in the interaction.
Main Methods:
- Utilized A549 human respiratory epithelial cells and P. fluorescens AF181.
- Administered cytochalasin D and genistein to assess the role of cytoskeleton and tyrosine kinases.
- Performed gene silencing of Alpha(v)Beta5 integrins and vitronectin.
Main Results:
- Cytochalasin D and genistein significantly decreased P. fluorescens adherence and internalization.
- Gene silencing of Alpha(v)Beta5 integrins and vitronectin markedly reduced bacterial adherence and invasion.
- P. fluorescens AF181 specifically binds to A549 cells, modulating inflammatory responses.
Conclusions:
- Alpha(v)Beta5 integrins and their ligand vitronectin are key mediators of P. fluorescens AF181 adherence and invasion in human epithelial cells.
- The host cell cytoskeleton and tyrosine kinases are involved in this bacterial-host cell interaction.
- These findings highlight potential therapeutic targets for P. fluorescens infections.
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