Related Experiment Video

Updated: Nov 18, 2025

High-throughput Assay to Phenotype Salmonella enterica Typhimurium Association, Invasion, and Replication in Macrophages
11:10

High-throughput Assay to Phenotype Salmonella enterica Typhimurium Association, Invasion, and Replication in Macrophages

Published on: August 11, 2014

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Salmonella Typhimurium reprograms macrophage metabolism via T3SS effector SopE2 to promote intracellular replication

Lingyan Jiang1,2, Peisheng Wang1,2, Xiaorui Song1,2

  • 1The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Nankai University, Tianjin, China.

Nature Communications
|February 10, 2021
PubMed

Insights

Salmonella Typhimurium infection alters host cell metabolism, upregulating glycolysis and decreasing serine synthesis. This metabolic shift enhances bacterial growth and virulence by providing nutrients and activating key bacterial systems.

Area of Science:

  • Microbiology
  • Cell Biology
  • Metabolic Engineering

Background:

  • Salmonella Typhimurium is a pathogen that infects host macrophages.
  • Understanding host-pathogen metabolic interactions is crucial for controlling bacterial infections.

Purpose of the Study:

  • To investigate how Salmonella Typhimurium infection affects host macrophage metabolism.
  • To elucidate the mechanisms by which metabolic alterations promote bacterial replication and virulence.

Main Methods:

  • Analysis of host macrophage metabolic pathways during S. Typhimurium infection.
  • Identification of bacterial factors, such as SopE2, involved in metabolic manipulation.
  • Assessment of bacterial replication and virulence under various metabolic conditions and genetic manipulations.

Main Results:

  • S. Typhimurium infection upregulates glycolysis and decreases serine synthesis in macrophages, accumulating glycolytic intermediates.
  • Bacterial protein SopE2 mediates the observed metabolic changes.
  • Metabolic alterations facilitate bacterial nutrient uptake and upregulate the S. Typhimurium SPI-2 pathogenicity island.

Conclusions:

  • Host cell metabolic reprogramming by S. Typhimurium is a key factor in pathogenesis.
  • Targeting host glycolysis or bacterial nutrient utilization pathways can impair S. Typhimurium replication and virulence.

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