आईएसएसएन: 2471-9315
Kazunari Tanigawa, Yasuhiro Hayashi, Akira Kawashima, Mitsuo Kiriya, Yasuhiro Nakamura, Yoko Fujiwara, Yuqian Luo, Mariko Mikami, Ken Karasawa, Koichi Suzuki
Mycobacterium leprae (M. leprae), an obligate intracellular pathogen, is the causative agent of leprosy by parasitizing skin macrophages (histiocytes) in the dermis and Schwann cells in the peripheral nerves. Host cells hijacked by M. leprae accumulate large amounts of lipid droplets, which appear foamy in typical lepromatous leprosy tissue sections. In these cells, lipid synthesis is promoted and its degradation suppressed by changes in the gene expression profile. We have recently reported that M. leprae infection increases the accumulation of triacylglycerol in infected cells, which is important for the survival of bacilli. In this mini-review, we briefly summarize the mechanism of lipid accumulation in M. leprae-infected cells in relation to its intracellular parasitization and discuss the possibility of altering lipid metabolism as a novel therapeutic strategy for leprosy.