The tug-of-war over MTOR in Legionella infections
Authors:Stanimir S. Ivanov
doi: 10.15698/mic2017.02.559
Volume 4, pp. 67 to 68, published 30/01/2017.
Department of Microbiology and Immunology, Louisiana State University Health Sciences Center – Shreveport, Shreveport, LA 71130.
Keywords:
Legionella, macrophage, lipids, lipogenesis, intracellular pathogens, MTOR, PI3K, SREBP.
Corresponding Author(s):
Conflict of interest statement:
The author has declared that no competing interests exist.
Please cite this article as:
Stanimir S. Ivanov (2017). The tug-of-war over MTOR in Legionella infections. Microbial Cell 4(2): 67-68.
© 2017 Ivanov. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.
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.