Abstract
A ruptured bacteria-containing organelle within the cytosol of an infected eukaryotic cell frequently initiates host defense responses that restrict pathogen replication. Therefore, source for lipids must be found to accommodate the organelle membrane expansion required to support bacterial replication. How host cells are manipulated to provide lipids for the expansion of pathogen-occupied organelles is not well understood. By investigating the interaction between macrophages and the human pulmonary pathogen Legionella pneumophila we uncovered that the host metabolic checkpoint kinase Mechanistic target of rapamycin (MTOR) is a central regulator of the pathogen niche expansion program.
Highlights
We uncovered that mouse bone marrowderived macrophages (BMMs) infected with pathogenic Legionella suppress Mechanistic target of rapamycin (MTOR) to promote inflammation through a host-driven mechanism
In our recent study (Abshire et al, PLoS Pathogens 2016 Dec 12;12(12):e1006088) we identified the Toll-like Receptor (TLR) adaptor Myeloid differentiation primary response gene 88 (Myd88) as a critical factor mediating the host-induced MTOR suppression in Legionella-infected BMMs
If dietary lipids and de novo lipogenesis are functionally redundant for Legionella-containing vacuole (LCV) growth in mammalian macrophages one might wonder why Legionella has retained the capacity to activate MTOR? MTOR anabolic regulation is conserved in unicellular amoebae, the natural hosts for Legionella, MICROREVIEW on: Abshire CF, Dragoi AM, Roy CR, Ivanov SS (2016)
Summary
We uncovered that mouse bone marrowderived macrophages (BMMs) infected with pathogenic Legionella suppress MTOR to promote inflammation through a host-driven mechanism. A ruptured bacteria-containing organelle within the cytosol of an infected eukaryotic cell frequently initiates host defense responses that restrict pathogen replication. Source for lipids must be found to accommodate the organelle membrane expansion required to support bacterial replication.
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