Many successful intracellular bacterial pathogens exploit nutrients and metabolites available in host cells to benefit colonization and replication. Despite significant advances in other areas of host-pathogen interactions made thus far, the mechanisms involved in the acquisition of nutrients and alteration of host cell metabolism are understudied.
Mechanisms involved can be divided into two: the scavenge/salvage pathway and de novo biosynthesis of molecules, which are often associated with bacteria-driven subversion of host cell metabolism. In general, obligate intracellular bacteria, including Chlamydiae and Rickettsiae, depend heavily on the scavenge/salvage pathway in exploiting host-derived metabolites due to the lack of genes required for de novo biosynthesis. In contrast, many facultative intracellular pathogens often use both mechanisms during their vacuolar and/or cytosolic lifecycles. For instance, vacuolar bacteria (e.g., Legionella pneumophila, Mycobacterium tuberculosis, Coxiella burnetti, Salmonella typhimurium) and cytosolic bacteria (e.g., Listeria monocytogenes, Shigella flexneri, Francisella tularensis) are known to target the central eukaryotic anabolic checkpoint pathway PI3K/AKT/mTOR, which orchestrates the biosynthesis of fatty acids, lipids and nucleotides in host cells. In addition, several vacuolar pathogens such as Mycobacterium tuberculosis and Salmonella typhimurium are known to activate HIF-1a to promote glucose uptake in infected host cells. It is highly anticipated that many mechanisms are involved in the process of repurposing host metabolites for bacterial replication and niche adaptation. Understanding these multifaceted strategies employed by intracellular bacterial pathogens will offer insights into developing new intervention strategies targeting this particular aspect of host-pathogen interactions.
In this Research Topic, we hope to put together research findings and insights concerning the mechanisms of how bacterial pathogens reprogram host metabolic pathways in vitro and in vivo. We welcome original research findings and analyses on how bacterial pathogens fine-tune host metabolisms to benefit their intracellular lifecycle. We particularly welcome contributions that include, but are not limited to, the following topics:
1. Common and unique strategies employed by bacteria to modulate host metabolisms during acute and chronic infections.
2. Metabolomic studies of facultative and obligate intracellular bacterial pathogens.
3. Dual RNA sequencing studies highlighting the transcriptional reprogramming of metabolic genes in the host and pathogen at different infectious stages.
4. Potential drug therapies targeting metabolic pathways required for persistent infection.
5. Metabolic switches employed by bacteria to adapt to different host cells and/or niches.
Submissions are welcome for the following article types:
1. Original research articles focusing on a new host and/or pathogen mechanism of their metabolic change processes in the context of infection.
2. Reviews, Mini-Reviews, or Perspectives summarizing relevant published work and providing insights into future directions.
3. Brief Research Reports and Hypotheses and Theory documenting preliminary findings with scientifically valid data driving potential new hypotheses in the field.
Many successful intracellular bacterial pathogens exploit nutrients and metabolites available in host cells to benefit colonization and replication. Despite significant advances in other areas of host-pathogen interactions made thus far, the mechanisms involved in the acquisition of nutrients and alteration of host cell metabolism are understudied.
Mechanisms involved can be divided into two: the scavenge/salvage pathway and de novo biosynthesis of molecules, which are often associated with bacteria-driven subversion of host cell metabolism. In general, obligate intracellular bacteria, including Chlamydiae and Rickettsiae, depend heavily on the scavenge/salvage pathway in exploiting host-derived metabolites due to the lack of genes required for de novo biosynthesis. In contrast, many facultative intracellular pathogens often use both mechanisms during their vacuolar and/or cytosolic lifecycles. For instance, vacuolar bacteria (e.g., Legionella pneumophila, Mycobacterium tuberculosis, Coxiella burnetti, Salmonella typhimurium) and cytosolic bacteria (e.g., Listeria monocytogenes, Shigella flexneri, Francisella tularensis) are known to target the central eukaryotic anabolic checkpoint pathway PI3K/AKT/mTOR, which orchestrates the biosynthesis of fatty acids, lipids and nucleotides in host cells. In addition, several vacuolar pathogens such as Mycobacterium tuberculosis and Salmonella typhimurium are known to activate HIF-1a to promote glucose uptake in infected host cells. It is highly anticipated that many mechanisms are involved in the process of repurposing host metabolites for bacterial replication and niche adaptation. Understanding these multifaceted strategies employed by intracellular bacterial pathogens will offer insights into developing new intervention strategies targeting this particular aspect of host-pathogen interactions.
In this Research Topic, we hope to put together research findings and insights concerning the mechanisms of how bacterial pathogens reprogram host metabolic pathways in vitro and in vivo. We welcome original research findings and analyses on how bacterial pathogens fine-tune host metabolisms to benefit their intracellular lifecycle. We particularly welcome contributions that include, but are not limited to, the following topics:
1. Common and unique strategies employed by bacteria to modulate host metabolisms during acute and chronic infections.
2. Metabolomic studies of facultative and obligate intracellular bacterial pathogens.
3. Dual RNA sequencing studies highlighting the transcriptional reprogramming of metabolic genes in the host and pathogen at different infectious stages.
4. Potential drug therapies targeting metabolic pathways required for persistent infection.
5. Metabolic switches employed by bacteria to adapt to different host cells and/or niches.
Submissions are welcome for the following article types:
1. Original research articles focusing on a new host and/or pathogen mechanism of their metabolic change processes in the context of infection.
2. Reviews, Mini-Reviews, or Perspectives summarizing relevant published work and providing insights into future directions.
3. Brief Research Reports and Hypotheses and Theory documenting preliminary findings with scientifically valid data driving potential new hypotheses in the field.