Outer membrane channel protein MctB in Mycobacterium tuberculosis is part of a Cu resistance mechanism that ensures low intracellular Cu levels in the bacterium. Human resisitance to bacteria, mediated via IFN-gamma-mediated activation of macrophages, may involve the use of reactive Cu(1) in the presence of hyrodgen peroxide, since acitivated Cu is toxic to bacteria. IFN-gamma stimulates the trafficking of the Cu transporter ATP7a to the vesicles that fuse with phagosomes and these phagosomes are found to have a high Cu content and an increaseed bactericidal activity against E.coli. Using MctB, Mycobacterium tuberculosis may limit the amount of excess Cu within it whole in the host.
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