Abstract
Pseudomonas aeruginosa PAO1 lon mutants are supersusceptible to ciprofloxacin, and exhibit a defect in cell division and in virulence-related properties, such as swarming, twitching and biofilm formation, despite the fact that the Lon protease is not a traditional regulator. Here we set out to investigate the influence of a lon mutation in a series of infection models. It was demonstrated that the lon mutant had a defect in cytotoxicity towards epithelial cells, was less virulent in an amoeba model as well as a mouse acute lung infection model, and impacted on in vivo survival in a rat model of chronic infection. Using qRT-PCR it was demonstrated that the lon mutation led to a down-regulation of Type III secretion genes. The Lon protease also influenced motility and biofilm formation in a mucin-rich environment. Thus alterations in several virulence-related processes in vitro in a lon mutant were reflected by defective virulence in vivo.
Highlights
Pseudomonas aeruginosa is a versatile Gram-negative bacterium that is found in many natural environments and causes infections of animals and plants [1]
The amoeba model was performed on the PA14 wildtype and lon mutant strains in order to confirm the results observed in the PAO1 background
Our results provided insights regarding the importance of the Lon protease of P. aeruginosa in virulence
Summary
Pseudomonas aeruginosa is a versatile Gram-negative bacterium that is found in many natural environments (including soils and marshes) and causes infections of animals and plants [1]. P. aeruginosa is a major opportunistic human pathogen, being the third most common cause of nosocomial infections. It can cause pneumonia, urinary-tract infections and bacteremia, as well as morbidity and mortality in cystic fibrosis (CF) patients due to chronic infections that eventually lead to lung damage and respiratory failure. Pseudomonas can form biofilms in the lung [3] This social behaviour enables the organism to resist clearance by the immune system, since organisms in biofilms are not accessible to phagocytes, and in addition bacteria growing in a biofilm are substantially more resistant to antimicrobial agents [4,5,6]. In chronically infected patients, where P. aeruginosa is thought to grow as biofilms, the bacteria are highly adaptively resistant to antimicrobial treatment, making eradication very difficult
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