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Updated: Jul 26, 2026
High-throughput Assay to Phenotype Salmonella enterica Typhimurium Association, Invasion, and Replication in Macrophages
Published on: August 11, 2014
The Salmonella virulence plasmid spv genes are required for cytopathology in human monocyte-derived macrophages
S J Libby1, M Lesnick, P Hasegawa
1Department of Microbiology, North Carolina State University, Raleigh 27695-7615, USA.
Abstract:
The pathogenesis of serious systemic Salmonella infections is characterized by survival and proliferation of bacteria inside macrophages. Infection of human monocyte-derived macrophages in vitro with S. typhimurium or S. dublin produces cytopathology characterized by detachment of cells that contain large numbers of proliferating bacteria. This cytopathology is dependent on the expression of the bacterial spv genes, a virulence locus previously shown to markedly enhance the ability of Salmonella to produce systemic disease. After 24 h of infection, macrophage cultures contain two populations of bacteria: (i) proliferating organisms present in a detached cell fraction; and (ii) a static bacterial population in macrophages remaining attached to the culture well. Mutations in either the essential transcriptional activator SpvR or the key SpvB protein markedly reduce the cytopathic effect of Salmonella infection. The spv-dependent cytopathology in macrophages exhibits characteristics of apoptosis, with release of nucleosomes into the cytoplasm, nuclear condensation and DNA fragmentation. The current findings suggest that the mechanism of the spv effect is through induction of increased cytopathology in host macrophages.
Insights
Salmonella typhimurium and Salmonella dublin infections cause cell damage in macrophages, driven by bacterial spv genes. These genes induce apoptosis, leading to systemic disease development.
Area of Science:
- Microbiology
- Immunology
- Bacterial Pathogenesis
Background:
- Systemic Salmonella infections involve bacterial survival and proliferation within macrophages.
- Salmonella typhimurium and Salmonella dublin infections in macrophages cause cytopathology and bacterial proliferation.
Purpose of the Study:
- To investigate the role of bacterial spv genes in Salmonella-induced macrophage cytopathology.
- To elucidate the mechanism by which spv genes contribute to systemic Salmonella infections.
Main Methods:
- In vitro infection of human monocyte-derived macrophages with S. typhimurium and S. dublin.
- Analysis of bacterial populations (proliferating vs. static) within macrophages.
- Assessment of cytopathology and apoptosis markers (nucleosome release, nuclear condensation, DNA fragmentation).
- Use of mutant strains with deletions in spvR and spvB genes.
Main Results:
- Salmonella-induced cytopathology in macrophages is dependent on the expression of spv genes.
- Two bacterial populations were observed: proliferating in detached cells and static in attached cells.
- Mutations in spvR or spvB significantly reduced the cytopathic effect.
- spv-dependent cytopathology exhibited characteristics of apoptosis.
Conclusions:
- The spv genes are crucial for Salmonella-induced macrophage cytopathology.
- The spv gene products likely induce apoptosis in host macrophages, contributing to systemic disease.
- Understanding the spv mechanism offers insights into Salmonella pathogenesis.
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