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Updated: May 13, 2026

Oral Transmission of Listeria monocytogenes in Mice via Ingestion of Contaminated Food
Published on: May 6, 2013
Listeria monocytogenes ArcA contributes to acid tolerance
Changyong Cheng1, Jianshun Chen2, Ying Shan1
1Zhejiang University Institute of Preventive Veterinary Medicine and Zhejiang Provincial Key Laboratory of Preventive Veterinary Medicine, 388 Yuhangtang Road, Hangzhou, Zhejiang 310058, PR China.
Listeria monocytogenes requires the arcA gene for survival in acidic environments, such as the stomach. Deleting arcA reduces Listeria monocytogenes virulence in mice.
Area of Science:
- Microbiology
- Pathogen Biology
- Molecular Biology
Background:
- Listeria monocytogenes is a foodborne pathogen that colonizes the intestinal tract and can cause systemic infections.
- Survival and adaptation to the low pH of the stomach are critical for L. monocytogenes to establish infection.
- The arginine deiminase pathway is a known mechanism for acid tolerance in bacteria.
Purpose of the Study:
- To investigate the role of the L. monocytogenes gene lmo0043 (orthologue of arcA) in acid tolerance and virulence.
- To characterize the function of ArcA in surviving acidic conditions and its impact on infection models.
Main Methods:
- Gene sequence analysis to identify conserved motifs in lmo0043.
- In vitro growth assays under various acidic conditions (pH 5.5, pH 2.5).
- Murine infection models (gastric and intraperitoneal inoculation) to assess survival and bacterial load.
Main Results:
- Transcription of arcA increased significantly under acid stress (pH 4.8).
- Deletion of arcA impaired L. monocytogenes growth at pH 5.5 and reduced survival in synthetic gastric fluid (pH 2.5) and the murine stomach.
- Mice infected with an arcA deletion mutant showed significantly lower bacterial load in the spleen compared to wild-type.
Conclusions:
- L. monocytogenes arcA is essential for acid tolerance in vitro.
- ArcA plays a crucial role in gastric survival and contributes to virulence in a murine model.
- Genetic complementation restored the wild-type phenotype, confirming arcA's role.
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