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Updated: May 5, 2026

Measuring Bacterial Load and Immune Responses in Mice Infected with Listeria monocytogenes
Published on: August 9, 2011
EⅡB Mutation Reduces the Pathogenicity of Listeria monocytogenes by Negatively Regulating Biofilm Formation Ability,
Caixia Liu1, Ruixuan Qian1, Weidi Shi1
1College of Animal Science and Technology, Shihezi University, Shihezi 832000, China.
Abstract:
To explore the role of the membrane permease ⅡB (EⅡB) gene of Listeria pathogenicity island 4 (LIPI-4) in the virulence of Listeria monocytogenes, both an EⅡB deletion strain (∆EⅡB) and a complemented strain were constructed. In vitro experiments demonstrated that EⅡB deletion affected the biofilm formation ability of the wild-type strain (Lm928). Moreover, this deletion decreased the intracellular proliferation abilities of L. monocytogenes. Mice infected with ∆EⅡB survived longer and experienced less weight loss on days 1, 2, and 3 post-infection. The bacterial load in the liver tissue of ∆EⅡB-infected mice was significantly reduced, and a considerable decrease in the blood levels of inflammatory cytokines IL-β, IL-6, IL-10, and TNF-α were observed. Following EⅡB deletion, 65% (13/20) of genes were downregulated, 25% (5/20) were upregulated, and 10% (2/20) showed no change. These findings suggest that EⅡB deletion may reduce both the in vivo and in vitro virulence levels as well as the biofilm formation ability of Lm928 by downregulating the transcription levels of genes associated with virulence and biofilm formation. These findings provide a foundation for further examining the pathogenic mechanisms of LIPI-4 and EⅡB in L. monocytogenes.
Insights
The membrane permease IIB (EIIB) gene deletion in Listeria monocytogenes reduced its virulence and biofilm formation. This EIIB gene plays a key role in Listeria pathogenicity.
Area of Science:
- Microbiology
- Molecular Biology
- Pathogenesis
Background:
- Listeria monocytogenes is a significant foodborne pathogen.
- The Listeria pathogenicity island 4 (LIPI-4) is crucial for L. monocytogenes virulence.
- The specific role of the EIIB gene within LIPI-4 requires further elucidation.
Purpose of the Study:
- To investigate the function of the membrane permease IIB (EIIB) gene from LIPI-4 in L. monocytogenes virulence.
- To assess the impact of EIIB deletion on bacterial behavior in vitro and in vivo.
Main Methods:
- Construction of an EIIB deletion strain (ΔEIIB) and a complemented strain.
- In vitro assays for biofilm formation and intracellular proliferation.
- In vivo infection model using mice to evaluate survival, weight loss, bacterial load, and cytokine levels.
- Transcriptomic analysis to identify gene expression changes post-EIIB deletion.
Main Results:
- EIIB deletion significantly impaired biofilm formation and intracellular proliferation of L. monocytogenes.
- Mice infected with ΔEIIB showed increased survival rates and reduced weight loss.
- Reduced bacterial load in liver tissue and decreased inflammatory cytokine levels (IL-1β, IL-6, IL-10, TNF-α) were observed in ΔEIIB infected mice.
- Gene expression analysis revealed widespread downregulation of virulence and biofilm-related genes following EIIB deletion.
Conclusions:
- The EIIB gene is essential for L. monocytogenes virulence and biofilm formation.
- EIIB deletion attenuates L. monocytogenes pathogenicity both in vitro and in vivo.
- Downregulation of virulence and biofilm genes is a key mechanism by which EIIB deletion reduces pathogenicity.
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