Control of iron metabolism in Mycobacterium tuberculosis.
Tuberculosis continues to kill millions of people around the world. New tools to prevent and treat this disease are urgently needed. Similar to most microorganisms, Mycobacterium tuberculosis--the causative agent of tuberculosis--requires iron for essential metabolic pathways. Because iron is not freely available in the host, pathogens must actively compete for this metal to establish an infection but they must also carefully control iron acquisition as excess free iron can be extremely toxic. Recent studies have demonstrated that failure to assemble the iron acquisition machinery or to repress iron uptake has deleterious effects for M. tuberculosis. Here, we review how M. tuberculosis obtains iron in a regulated manner and discuss how these processes could potentially be disrupted to interfere with the survival and replication of this bacterium in the host.
Rodriguez
G Marcela
GM
TB Center, The Public Health Research Institute at the International Center for Public Health, 225 Warren St, Newark, NJ 07103, USA. marcela@phri.org
D001426:Bacterial Proteins / Q000737:chemistry / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D001692:Biological Transport / Q000235:genetics / Q000502:physiology; D015195:Drug Design; D006706:Homeostasis; D007501:Iron / Q000737:chemistry / Q000378:metabolism*; D008954:Models, Biological; D008958:Models, Molecular; D009169:Mycobacterium tuberculosis / Q000378:metabolism* / Q000472:pathogenicity / Q000502:physiology; D010080:Oxazoles / Q000737:chemistry / Q000378:metabolism; D012097:Repressor Proteins / Q000737:chemistry / Q000235:genetics / Q000502:physiology
D001426:Bacterial Proteins; C096348:IdeR protein, Mycobacterium tuberculosis; D010080:Oxazoles; D012097:Repressor Proteins; C018608:mycobactins; D007501:Iron