The formation of lipid droplets favors intracellular Mycobacterium leprae survival in SW-10, non-myelinating Schwann cells.
The formation of lipid droplets favors intracellular Mycobacterium leprae survival in SW-10, non-myelinating Schwann cells.
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DOI：
10.1371/journal.pntd.0005687
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发表时间：
2017-06
影响因子：
3.8
通讯作者：
Lee SB
中科院分区：
文献类型：
--
作者：
Jin SH;An SK;Lee SB
麻风病是由专性胞内病原体麻风分枝杆菌（M.leprae）引起的慢性传染病，其是全世界所有非创伤性周围神经病变的主要原因。虽然在瘤型麻风患者中，有髓鞘和无髓鞘的雪旺细胞都被麻风分枝杆菌感染，但麻风分枝杆菌优先侵袭无髓鞘的雪旺细胞。然而，麻风分枝杆菌感染对非髓鞘化雪旺细胞的影响尚未阐明。在瘤型麻风患者的神经活检中，在麻风杆菌感染的许旺细胞中发现了脂滴（LD）。麻风分枝杆菌诱导的LD形成有利于胞内麻风分枝杆菌在原代许旺细胞和称为ST 88 -14的髓鞘形成许旺细胞系中的存活。在目前的研究中，我们首先表征了SW-10细胞，并研究了LD对麻风杆菌感染的SW-10细胞（非髓鞘形成的许旺细胞）的影响。SW-10细胞表达S100和NGFR p75，S100是神经嵴细胞的标志物，NGFR p75是未成熟或非髓鞘形成的许旺细胞的标志物。然而，SW-10细胞不表达髓鞘碱性蛋白（MBP）（髓鞘形成许旺细胞的标志物）和髓鞘蛋白零（MPZ）（前体、未成熟或髓鞘形成许旺细胞的标志物），所有这些都表明SW-10细胞是非髓鞘形成许旺细胞。此外，SW-10细胞具有吞噬活性，可被M.麻风病人杆菌感染麻风病诱导LD的形成。抑制M.麻风诱导的LD促进了含有活麻风分枝杆菌的吞噬体的成熟，并降低了M.在SW-10细胞中发现麻风。这些事实表明，LD形成M。麻风病倾向于细胞内M.这导致了合乎逻辑的结论，即麻风分枝杆菌感染的SW-10细胞可以成为研究麻风分枝杆菌与非髓鞘化雪旺细胞相互作用的新模型。麻风病是一种由专性胞内病原体麻风分枝杆菌（M.leprae）引起的慢性传染病。麻风病是全世界所有非创伤性周围神经病变的主要原因。在瘤型麻风中，髓鞘形成和非髓鞘形成的雪旺细胞都受到麻风分枝杆菌的感染，但非髓鞘形成的雪旺细胞对麻风分枝杆菌的侵袭表现出更大的易感性。然而，麻风分枝杆菌感染对非髓鞘化雪旺细胞的影响尚未阐明。我们的结果表明SW-10细胞是非髓鞘形成的雪旺细胞。杆菌感染麻风诱导脂滴（LD）形成。此外，抑制M.麻风诱导的LD形成促进了含有活麻风分枝杆菌的吞噬体的成熟，并降低了麻风分枝杆菌的ATP含量。在SW-10细胞中，M.麻风病人喜欢M. SW-10细胞中的麻风存活率。基于这些发现，应该清楚的是，麻风分枝杆菌感染的SW-10细胞可以作为研究麻风分枝杆菌与非髓鞘化雪旺细胞相互作用的新模型。
Leprosy is a chronic infectious disease that is caused by the obligate intracellular pathogen Mycobacterium leprae (M.leprae), which is the leading cause of all non-traumatic peripheral neuropathies worldwide. Although both myelinating and non-myelinating Schwann cells are infected by M.leprae in patients with lepromatous leprosy, M.leprae preferentially invades the non-myelinating Schwann cells. However, the effect of M.leprae infection on non-myelinating Schwann cells has not been elucidated. Lipid droplets (LDs) are found in M.leprae-infected Schwann cells in the nerve biopsies of lepromatous leprosy patients. M.leprae-induced LD formation favors intracellular M.leprae survival in primary Schwann cells and in a myelinating Schwann cell line referred to as ST88-14. In the current study, we initially characterized SW-10 cells and investigated the effects of LDs on M.leprae-infected SW-10 cells, which are non-myelinating Schwann cells. SW-10 cells express S100, a marker for cells from the neural crest, and NGFR p75, a marker for immature or non-myelinating Schwann cells. SW-10 cells, however, do not express myelin basic protein (MBP), a marker for myelinating Schwann cells, and myelin protein zero (MPZ), a marker for precursor, immature, or myelinating Schwann cells, all of which suggests that SW-10 cells are non-myelinating Schwann cells. In addition, SW-10 cells have phagocytic activity and can be infected with M. leprae. Infection with M. leprae induces the formation of LDs. Furthermore, inhibiting the formation of M. leprae-induced LD enhances the maturation of phagosomes containing live M.leprae and decreases the ATP content in the M. leprae found in SW-10 cells. These facts suggest that LD formation by M. leprae favors intracellular M. leprae survival in SW-10 cells, which leads to the logical conclusion that M.leprae-infected SW-10 cells can be a new model for investigating the interaction of M.leprae with non-myelinating Schwann cells. Leprosy is a chronic infectious disease that is caused by the obligate intracellular pathogen Mycobacterium leprae (M.leprae). Leprosy is the leading cause of all non-traumatic peripheral neuropathies worldwide. Both myelinating and non-myelinating Schwann cells are infected by M.leprae in lepromatous leprosy, but the non-myelinating Schwann cells show greater susceptibility to M.leprae invasion. However, the effect of M.leprae infection on non-myelinating Schwann cells has not been elucidated. Our results show that SW-10 cells are non-myelinating Schwann cells. Infection with M. leprae induces lipid droplet (LD) formation. Furthermore, inhibition of M. leprae-induced LD formation enhances the maturation of phagosomes containing live M.leprae and decreases the ATP content of M. leprae in SW-10 cells, suggesting that LD formation by M. leprae favors M. leprae survival in SW-10 cells. Based on these findings, it should be clear that M.leprae-infected SW-10 cells can serve as a new model for investigating the interaction of M.leprae with non-myelinating Schwann cells.