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Updated: Aug 10, 2026

Measuring Bacterial Load and Immune Responses in Mice Infected with Listeria monocytogenes
Published on: August 9, 2011
[Effect of the constitutive activity of pathogenicity genes in Listeria monocytogenes]
Abstract:
The effect of the constitutive expression of pathogenicity factors in L. monocytogenes was studied on the model of the intraperitoneal infection of mice. The constitutive expression was due to a single amino acid substitution in the transcriptional factor PfrA, the master regulator of L. monocytogenes virulence genes. The effective lethal dose (LD50) for the strain with the constitutive expression of pathogenicity factors was 3 times lower than for the isogenic wildtype strain. When introduced in equal doses, this Listeria strain led to the death of the animals 1-2 days earlier than the wild-type stain. The study revealed that the constitutive expression of pathogenicity factors resulted in faster dissemination of bacteria in the body of the animal during the first 24 hours, but led to their earlier elimination from the internal organs at later stages of infection.
Insights
Constitutive expression of Listeria monocytogenes virulence factors, regulated by PfrA, significantly increased bacterial lethality in mice. This enhanced virulence led to faster dissemination but earlier clearance from organs.
Area of Science:
- Microbiology
- Infectious Diseases
- Bacterial Pathogenesis
Background:
- Listeria monocytogenes is a significant foodborne pathogen.
- Virulence gene regulation is crucial for L. monocytogenes pathogenesis.
- The transcriptional factor PfrA controls L. monocytogenes virulence.
Purpose of the Study:
- To investigate the impact of constitutive pathogenicity factor expression in L. monocytogenes.
- To determine the role of PfrA in regulating virulence gene expression.
- To assess the in vivo effects of enhanced virulence on mouse models.
Main Methods:
- Generating a L. monocytogenes strain with constitutive expression of virulence factors via a PfrA mutation.
- Intraperitoneal infection of mice with the engineered strain and wild-type controls.
- Determining the lethal dose 50 (LD50) and survival rates.
- Monitoring bacterial dissemination and organ clearance.
Main Results:
- The PfrA-mutated strain exhibited a 3-fold lower LD50 compared to the wild-type.
- Mice infected with the engineered strain died 1-2 days earlier.
- Faster bacterial dissemination within the first 24 hours post-infection was observed.
- Earlier elimination of bacteria from internal organs at later infection stages.
Conclusions:
- Constitutive expression of L. monocytogenes pathogenicity factors enhances virulence and lethality.
- PfrA plays a critical role in the temporal regulation of virulence.
- Altered bacterial kinetics, including dissemination and clearance, impact infection outcome.
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