Mechanism of Inducible Nitric Oxide Synthase Exclusion from Mycobacterial Phagosomes

• Published in: PLoS pathogens Vol. 3; no. 12; p. e186
• Main Authors: Davis, Alexander S, Vergne, Isabelle, Master, Sharon S, Kyei, George B, Chua, Jennifer, Deretic, Vojo
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 01.12.2007; Public Library of Science (PLoS)
• Subjects: Actins - metabolism; Animals; Binding Sites; Cell Line; Coronin; Cytoskeleton - metabolism; Enzymes; Ezrin-Binding Protein 50; Gene Silencing; Host-Pathogen Interactions - drug effects; Host-Pathogen Interactions - physiology; Interferon-gamma - pharmacology; Latex; Lipopolysaccharides - pharmacology; Macrophage; Macrophage Activation; Macrophages - drug effects; Macrophages - enzymology; Macrophages - microbiology; Mice; Mice, Inbred C57BL; Mice, Knockout; Microbial Viability; Microbiology; Mycobacterium; Mycobacterium - physiology; Mycobacterium bovis - metabolism; Mycobacterium bovis - pathogenicity; Mycobacterium tuberculosis; Mycobacterium tuberculosis - metabolism; Mycobacterium tuberculosis - pathogenicity; Nitric oxide; Nitric Oxide Synthase; Nitric Oxide Synthase Type II - deficiency; Nitric Oxide Synthase Type II - genetics; Nitric Oxide Synthase Type II - metabolism; Phagosomes - enzymology; Phagosomes - immunology; Phosphoproteins; RNA, Small Interfering - genetics; Rodents; Sodium-Hydrogen Exchangers; Tuberculosis

Mycobacterium tuberculosis is sensitive to nitric oxide generated by inducible nitric oxide synthase (iNOS). Consequently, to ensure its survival in macrophages, M. tuberculosis inhibits iNOS recruitment to its phagosome by an unknown mechanism. Here we report the mechanism underlying this process,...