Inactivation of phospholipase D diminishes Acinetobacter baumannii pathogenesis
Anna C Jacobs1, Indriati Hood, Kelli L Boyd
1Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198-5900, USA.
Abstract:
Acinetobacter baumannii is an emerging bacterial pathogen of considerable health care concern. Nonetheless, relatively little is known about the organism's virulence factors or their regulatory networks. Septicemia and ventilator-associated pneumonia are two of the more severe forms of A. baumannii disease. To identify virulence factors that may contribute to these disease processes, genetically diverse A. baumannii clinical isolates were evaluated for the ability to proliferate in human serum. A transposon mutant library was created in a strain background that propagated well in serum and screened for members with decreased serum growth. The results revealed that disruption of A. baumannii phospholipase D (PLD) caused a reduction in the organism's ability to thrive in serum, a deficiency in epithelial cell invasion, and diminished pathogenesis in a murine model of pneumonia. Collectively, these results suggest that PLD is an A. baumannii virulence factor.
Insights
Acinetobacter baumannii phospholipase D (PLD) is a key virulence factor. Disrupting PLD reduced bacterial growth in serum, invasion of host cells, and disease severity in a pneumonia model.
Area of Science:
- Microbiology
- Infectious Diseases
- Bacterial Pathogenesis
Background:
- Acinetobacter baumannii is a significant healthcare-associated pathogen.
- Limited knowledge exists regarding its virulence factors and regulatory mechanisms.
- Severe diseases include septicemia and ventilator-associated pneumonia.
Purpose of the Study:
- To identify novel virulence factors of Acinetobacter baumannii.
- To investigate factors contributing to severe disease forms like pneumonia.
Main Methods:
- Created a transposon mutant library in a serum-resistant A. baumannii strain.
- Screened the library for mutants with reduced growth in human serum.
- Evaluated mutant phenotypes for epithelial cell invasion and a murine pneumonia model.
Main Results:
- Disruption of phospholipase D (PLD) significantly reduced bacterial survival in serum.
- PLD-deficient mutants showed impaired epithelial cell invasion.
- Pathogenesis in a murine pneumonia model was diminished in the absence of PLD.
Conclusions:
- Phospholipase D (PLD) is identified as a crucial virulence factor for Acinetobacter baumannii.
- PLD contributes to bacterial serum resistance, host cell invasion, and overall disease progression.
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