Bacterial persistence: finding the "sweet spot"

R Martin Roop1, Clayton C Caswell

  • 1Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC 27858, USA. roopr@ecu.edu

Cell Host & Microbe
|August 20, 2013
PubMed

Insights

Bacterial pathogens Salmonella and Brucella use increased glucose in alternatively activated macrophages to prolong chronic infections in mice. This highlights a key metabolic vulnerability exploited by these bacteria.

Area of Science:

  • Immunology
  • Microbiology
  • Metabolic pathways

Background:

  • Alternatively activated macrophages (AAMs) are crucial in host defense and tissue repair.
  • Chronic infections by bacterial pathogens pose significant public health challenges.
  • Metabolic reprogramming of immune cells influences host-pathogen interactions.

Purpose of the Study:

  • To investigate the metabolic adaptations of macrophages during chronic bacterial infections.
  • To identify specific nutrients exploited by Salmonella and Brucella within the host environment.
  • To understand how macrophage polarization impacts susceptibility to infection.

Main Methods:

  • Experimental infection of mice with Salmonella and Brucella.
  • Analysis of macrophage metabolic profiles, including glucose uptake and utilization.
  • In vivo and in vitro assays to assess bacterial growth and survival in different macrophage subsets.

Main Results:

  • Alternatively activated macrophages exhibit significantly higher glucose levels compared to other macrophage subsets.
  • Salmonella and Brucella actively utilize this increased glucose to fuel their replication and persistence.
  • Depletion of glucose or inhibition of its uptake impairs bacterial chronic infection.

Conclusions:

  • Glucose availability in alternatively activated macrophages is a critical factor for sustaining chronic Salmonella and Brucella infections.
  • Targeting macrophage glucose metabolism represents a potential therapeutic strategy against these pathogens.
  • This study reveals a novel mechanism of host-pathogen metabolic interplay.

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