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LACTATEing Salmonella: A Host-Derived Fermentation Product Fuels Pathogen Growth
Bärbel Stecher1, Kirsten Jung2
1Max von Pettenkofer Institute of Hygiene and Medical Microbiology, Faculty of Medicine, LMU Munich, Pettenkoferstr. 9a, 80336 Munich, Germany; German Center for Infection Research (DZIF), Partner Site LMU Munich, Munich, Germany.
Cell Host & Microbe
|January 12, 2018
Summary
Salmonella infection reduces beneficial butyrate, causing colon cells to ferment lactate. This lactate then fuels Salmonella growth, worsening the infection. Understanding this metabolic shift is key to fighting Salmonella.
Area of Science:
- Microbiology
- Host-Microbe Interactions
- Metabolic Reprogramming
Background:
- Salmonella enterica serovar Typhimurium infection causes gut dysbiosis.
- Microbiota-derived butyrate levels decrease during Salmonella infection.
Purpose of the Study:
- To investigate the metabolic consequences of reduced butyrate during Salmonella infection.
- To elucidate the role of colonic epithelial metabolism in supporting Salmonella growth.
Main Methods:
- Analysis of colonic epithelial metabolism during Salmonella infection.
- Investigating the utilization of fermentation products by Salmonella.
Main Results:
- Reduced butyrate reprograms colonic epithelial cells to ferment lactate.
- Lactate produced by epithelial cells serves as a respiratory electron donor for Salmonella.
- This metabolic adaptation supports Salmonella growth and promotes infection.
Conclusions:
- Butyrate depletion is a critical factor in Salmonella-induced metabolic changes.
- Colonic lactate fermentation is a key mechanism supporting Salmonella pathogenesis.
- Targeting host metabolic reprogramming could be a therapeutic strategy against Salmonella.
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