English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Francisella tularensis  is a highly infectious Gram-negative bacterium and the causative agent of the zoonotic disease tularemia. This bacterial pathogen can infect a broad variety of animal species and can be transmitted to humans in numerous ways with various clinical outcomes. Although,  Francisella  possesses the capacity to infect numerous mammalian cell types, the macrophage constitutes the main intracellular niche, used for  in vivo  bacterial dissemination. To survive and multiply within infected macrophages,  Francisella  must imperatively escape from the phagosomal compartment. In the cytosol, the bacterium needs to control the host innate immune response and adapt its metabolism to this nutrient-restricted niche. Our laboratory has shown that intracellular  Francisella  mainly relied on host amino acid as major gluconeogenic substrates and provided evidence that the host metabolism was also modified upon  Francisella  infection. We will review here our current understanding of how  Francisella  copes with the available nutrient sources provided by the host cell during the course of infection.

Importance of Metabolic Adaptations in Francisella Pathogenesis