title: Copper homeostasis in Mycobacterium tuberculosis.
abstract: Copper (Cu) is a trace element essential for the growth and development of almost all organisms, including bacteria. However, Cu overload in most systems is toxic. Studies show Cu accumulates in macrophage phagosomes infected with bacteria, suggesting Cu provides an innate immune mechanism to combat invading pathogens. To counteract the host-supplied Cu, increasing evidence suggests that bacteria have evolved Cu resistance mechanisms to facilitate their pathogenesis. In particular, Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis, has evolved multiple pathways to respond to Cu. Here, we summarize what is currently known about Cu homeostasis in Mtb and discuss potential sources of Cu encountered by this and other pathogens in a mammalian host.
authors.affiliation: New York University School of Medicine, Department of Microbiology, 550 First Avenue MSB 236, New York, NY 10016, USA. heran.darwin@med.nyu.edu.
authors.forename: Xiaoshan
authors.initials: X
authors.lastname: Shi
authors.forename: K Heran
authors.initials: KH
authors.lastname: Darwin
mesh_terms: D000818:Animals; D003300:Copper / Q000378:metabolism*; D006706:Homeostasis; D054884:Host-Pathogen Interactions; D006801:Humans; D042541:Intracellular Space / Q000382:microbiology; D009169:Mycobacterium tuberculosis / Q000502:physiology*; D014376:Tuberculosis / Q000382:microbiology / Q000473:pathology
chemical_list: D003300:Copper