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• W1991233072 abstract "A hallmark of tuberculosis is the ability of the causative agent, Mycobacterium tuberculosis, to persist for decades despite a vigorous host immune response. Previously, we identified a mycobacterial gene cluster, mce4, that was specifically required for bacterial survival during this prolonged infection. We now show that mce4 encodes a cholesterol import system that enables M. tuberculosis to derive both carbon and energy from this ubiquitous component of host membranes. Cholesterol import is not required for establishing infection in mice or for growth in resting macrophages. However, this function is essential for persistence in the lungs of chronically infected animals and for growth within the IFN-gamma-activated macrophages that predominate at this stage of infection. This finding indicates that a major effect of IFN-gamma stimulation may be to sequester potential pathogens in a compartment devoid of more commonly used nutrients. The unusual capacity to catabolize sterols allows M. tuberculosis to circumvent this defense and thereby sustain a persistent infection." @default.
• W1991233072 created "2016-06-24" @default.
• W1991233072 creator A5030420909 @default.
• W1991233072 creator A5062955181 @default.
• W1991233072 date "2008-03-18" @default.
• W1991233072 modified "2023-10-14" @default.
• W1991233072 title "Mycobacterial persistence requires the utilization of host cholesterol" @default.
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• W1991233072 doi "https://doi.org/10.1073/pnas.0711159105" @default.
• W1991233072 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2393810" @default.
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• W1991233072 hasPublicationYear "2008" @default.
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