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Summary  We recently showed that   M   ycobacterium leprae  ( ML ) is able to induce lipid droplet formation in infected macrophages. We herein confirm that cholesterol ( Cho ) is one of the host lipid molecules that accumulate in  ML ‐infected macrophages and investigate the effects of  ML  on cellular  Cho  metabolism responsible for its accumulation. The expression levels of  LDL  receptors ( LDL ‐ R ,  CD 36,  SRA ‐1,  SR ‐ B 1, and  LRP ‐1) and enzymes involved in  Cho  biosynthesis were investigated by  qRT ‐ PCR  and/or  W estern blot and shown to be higher in lepromatous leprosy ( LL ) tissues when compared to borderline tuberculoid ( BT ) lesions. Moreover, higher levels of the active form of the sterol regulatory element‐binding protein ( SREBP ) transcriptional factors, key regulators of the biosynthesis and uptake of cellular Cho, were found in  LL  skin biopsies. Functional  in vitro  assays confirmed the higher capacity of  ML ‐infected macrophages to synthesize  Cho  and sequester exogenous  LDL ‐ Cho . Notably,  Cho  colocalized to  ML ‐containing phagosomes, and  Cho  metabolism impairment, through either  de novo  synthesis inhibition by statins or depletion of exogenous  Cho , decreased intracellular bacterial survival. These findings highlight the importance of metabolic integration between the host and bacteria to leprosy pathophysiology, opening new avenues for novel therapeutic strategies to leprosy.

cellular microbiology

M   ycobacterium leprae  intracellular survival relies on cholesterol accumulation in infected macrophages: a potential target for new drugs for leprosy treatment