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The essential role of cholesterol metabolism in the intracellular survival of Mycobacterium leprae is not coupled to central carbon metabolism and energy production.

Abstract

Mycobacterium leprae induces the formation of lipid droplets, which are recruited to pathogen-containing phagosomes in infected macrophages and Schwann cells. Cholesterol is among the lipids with increased abundance in M. leprae infected cells, and intracellular survival relies on cholesterol accumulation.

However, the bacteria avidly incorporated cholesterol, and as expected, converted it to cholestenone both in vitro and in vivo. Our data indicate that M. leprae has lost the capacity to degrade and utilize cholesterol as a nutritional source, but retains the enzyme responsible for its oxidation to cholestenone. Thus, the essential role of cholesterol metabolism in the intracellular survival of M. leprae is uncoupled from central carbon metabolism and energy production. Further elucidation of cholesterol metabolism in the host cell during M. leprae infection will establish the mechanism by which this lipid supports M. leprae intracellular survival and will open new avenues for novel leprosy therapies.

More information

Type
Journal Article
Author
Marques MA
Berrêdo-Pinho M
Rosa T
Pujari V
Lemes R
Lery L
Silva CAM
Guimarães AC
Atella GC
Wheat W
Brennan PJ
Crick D
Belisle JT
Pessolani MC

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