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Selected Publication:
SHR Neuro Cancer Cardio Lipid Metab Microb
Kentner, D; Martano, G; Callon, M; Chiquet, P; Brodmann, M; Burton, O; Wahlander, A; Nanni, P; Delmotte, N; Grossmann, J; Limenitakis, J; Schlapbach, R; Kiefer, P; Vorholt, JA; Hiller, S; Bumann, D.
Shigella reroutes host cell central metabolism to obtain high-flux nutrient supply for vigorous intracellular growth.
Proc Natl Acad Sci U S A. 2014; 111(27):9929-9934
Doi: 10.1073/pnas.1406694111
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- Co-authors Med Uni Graz
- Brodmann Marianne
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- Abstract:
- Shigella flexneri proliferate in infected human epithelial cells at exceptionally high rates. This vigorous growth has important consequences for rapid progression to life-threatening bloody diarrhea, but the underlying metabolic mechanisms remain poorly understood. Here, we used metabolomics, proteomics, and genetic experiments to determine host and Shigella metabolism during infection in a cell culture model. The data suggest that infected host cells maintain largely normal fluxes through glycolytic pathways, but the entire output of these pathways is captured by Shigella, most likely in the form of pyruvate. This striking strategy provides Shigella with an abundant favorable energy source, while preserving host cell ATP generation, energy charge maintenance, and survival, despite ongoing vigorous exploitation. Shigella uses a simple three-step pathway to metabolize pyruvate at high rates with acetate as an excreted waste product. The crucial role of this pathway for Shigella intracellular growth suggests targets for antimicrobial chemotherapy of this devastating disease.
- Find related publications in this database (using NLM MeSH Indexing)
- Acetates - metabolism
- Carbon - metabolism
- Cell Division -
- Cytosol - metabolism
- Genome, Bacterial -
- HeLa Cells -
- Humans -
- Metabolomics -
- Nuclear Magnetic Resonance, Biomolecular -
- Oxygen - metabolism
- Pyruvic Acid - metabolism
- Shigella - genetics Shigella - metabolism Shigella - physiology
- Find related publications in this database (Keywords)
- infectious diseases
- host-pathogen interactions