01781nas a2200265   4500000000100000008004100001100001500042700002100057700001100078700001300089700001200102700001100114700001400125700001800139700001400157700001200171700001500183700001200198700001500210700001700225245017000242856004800412520104100460022001401501       2015                            d1 aMarques MA1 aBerrêdo-Pinho M1 aRosa T1 aPujari V1 aLemes R1 aLery L1 aSilva CAM1 aGuimarães AC1 aAtella GC1 aWheat W1 aBrennan PJ1 aCrick D1 aBelisle JT1 aPessolani MC00aThe essential role of cholesterol metabolism in the intracellular survival of Mycobacterium leprae is not coupled to central carbon metabolism and energy production.  uhttp://jb.asm.org/content/197/23/3698.full 3 a<p>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.</p>

<p>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.</p>
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