Washington State University
F. tularensis exploits AMPK activation to acquire host-derived nutrients
Francisella tularensis, a highly virulent bacterial pathogen, causes tularemia in humans. In humans, tularemia leads to acute infections, but chronic infections result in bacteremia and have a high chance of being fatal. With a low infectious dose and potential to be used as a bioterrorism weapon, F. tularensis poses a significant public health risk. During infection, F. tularensis encounters a wide range of environments within cells. Following entry into the cell and phagosome escape, the bacterium replicates rapidly in the cell cytoplasm. F. tularensis replication depends on the availability and use of various cellular nutrients. However, the mechanisms by which these nutrients become available to the bacterium is not fully understood. We found that F. tularensis infected cells had increased activation of adenosine monophosphate protein kinase (AMPK). Activated AMPK increased lipid degradation in infected cells. An increase in lipid droplet degradation allows F. tularensis to use carbon sources, such as fatty acids and glycerol, as energy for replication. Our findings suggest F. tularensis exploits AMPK activation to access nutrients sequestered in lipid droplets to undergo efficient bacterial replication that leads to a successful infection.
SACNAS Virtual National Diversity in STEM Conference, October 25-29, 2021