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Updated: Jul 14, 2025

High-throughput Assay to Phenotype Salmonella enterica Typhimurium Association, Invasion, and Replication in Macrophages
Published on: August 11, 2014
Lactate promotes Salmonella intracellular replication and systemic infection via driving macrophage M2 polarization
Xinyue Wang1, Bin Yang1, Shuangshuang Ma1,2
1The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, TEDA Institute of Biological Sciences and Biotechnology, Nankai University , Tianjin, China.
Importance:
The important enteropathogen Salmonella can cause lethal systemic infection via survival and replication in host macrophages. Lactate represents an abundant intracellular metabolite during bacterial infection, which can also induce macrophage M2 polarization. In this study, we found that macrophage-derived lactate promotes the intracellular replication and systemic infection of Salmonella. During Salmonella infection, lactate via the Salmonella type III secretion system effector SteE promotes macrophage M2 polarization, and the induction of macrophage M2 polarization by lactate is responsible for lactate-mediated Salmonella growth promotion. This study highlights the complex interactions between Salmonella and macrophages and provides an additional perspective on host-pathogen crosstalk at the metabolic interface.
Insights
Macrophage-derived lactate fuels Salmonella growth and systemic infection by promoting M2 polarization. This lactate-induced M2 polarization is key to Salmonella
Area of Science:
- Microbiology
- Immunology
- Metabolic pathways
Background:
- Salmonella is a major enteropathogen causing systemic infections via macrophage survival and replication.
- Lactate, an abundant metabolite during infection, can polarize macrophages towards an M2 phenotype.
Purpose of the Study:
- To investigate the role of macrophage-derived lactate in promoting Salmonella intracellular replication and systemic infection.
- To elucidate the mechanism by which lactate influences macrophage polarization and Salmonella growth.
Main Methods:
- Utilized Salmonella infection models in macrophages.
- Analyzed lactate production and its effect on macrophage M2 polarization.
- Investigated the involvement of the Salmonella type III secretion system effector SteE.
Main Results:
- Macrophage-derived lactate significantly promotes Salmonella intracellular replication and systemic infection.
- Lactate, via Salmonella effector SteE, induces macrophage M2 polarization.
- Lactate-mediated M2 polarization is essential for promoting Salmonella growth.
Conclusions:
- Macrophage lactate is a critical factor in enhancing Salmonella virulence.
- The interplay between lactate metabolism, macrophage polarization, and Salmonella pathogenesis offers new therapeutic targets.
- This study reveals a novel metabolic interface in host-pathogen interactions.
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