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Updated: Apr 17, 2026
Method for the Isolation of Francisella tularensis Outer Membranes
Published on: June 29, 2010
The complex amino acid diet of Francisella in infected macrophages
Monique Barel1, Elodie Ramond1, Gael Gesbert1
1Université Paris Descartes, Sorbonne Paris Cité Paris, France ; INSERM U1151 - Centre National de la Recherche Scientifique UMR 8253, Institut Necker-Enfants Malades Paris, France.
Abstract:
Francisella tularensis, the agent of the zoonotic disease tularemia, is a highly infectious bacterium for a large number of animal species and can be transmitted to humans by various means. The bacterium is able to infect a variety of cell types but replicates in mammalian hosts mainly in the cytosol of infected macrophages. In order to resist the stressful and nutrient-restricted intracellular environments, it encounters during its systemic dissemination, Francisella has developed dedicated stress resistance mechanisms and adapted its metabolic and nutritional needs. Recent data form our laboratory and from several other groups have shown that Francisella simultaneously relies on multiple host amino acid sources during its intracellular life cycle. This review will summarize how intracellular Francisella use different amino acid sources, and their role in phagosomal escape and/or cytosolic multiplication and systemic dissemination. We will first summarize the data that we have obtained on two amino acid transporters involved in Francisella phagosomal escape and cytosolic multiplication i.e., the glutamate transporter GadC and the asparagine transporter AnsP, respectively. The specific contribution of glutamate and asparagine to the physiology of the bacterium will be evoked. Then, we will discuss how Francisella has adapted to obtain and utilize host amino acid resources, and notably the contribution of host transporters and autophagy process in the establishment of a nutrient-replete intracellular niche.
Insights
Francisella tularensis bacteria utilize host amino acids for intracellular survival and replication. Key transporters like GadC and AnsP facilitate escape and multiplication within host cells.
Area of Science:
- Microbiology
- Infectious Diseases
- Cell Biology
Background:
- Francisella tularensis causes tularemia, a zoonotic disease.
- It infects various cell types, primarily replicating in macrophage cytosol.
- Intracellular survival requires adaptation to nutrient-limited environments.
Purpose of the Study:
- To review how intracellular Francisella utilizes host amino acids.
- To elucidate the role of amino acid sources in phagosomal escape and cytosolic multiplication.
- To discuss Francisella's adaptation to host nutrient acquisition.
Main Methods:
- Review of existing laboratory data and published research.
- Focus on specific amino acid transporters: glutamate transporter GadC and asparagine transporter AnsP.
- Analysis of host cell mechanisms, including transporters and autophagy.
Main Results:
- Francisella simultaneously relies on multiple host amino acid sources.
- Glutamate and asparagine play specific roles in bacterial physiology.
- Host transporters and autophagy contribute to nutrient availability in the intracellular niche.
Conclusions:
- Host amino acid acquisition is critical for Francisella intracellular survival and dissemination.
- Specific amino acid transporters are key for bacterial pathogenesis.
- Understanding these mechanisms can inform therapeutic strategies against tularemia.
