Abstract:
:Mycobacterium leprae causes leprosy and is unique among mycobacterial diseases in producing peripheral neuropathy. This debilitating morbidity is attributed to axon demyelination resulting from direct interaction of the M. leprae-specific phenolic glycolipid 1 (PGL-1) with myelinating glia and their subsequent infection. Here, we use transparent zebrafish larvae to visualize the earliest events of M. leprae-induced nerve damage. We find that demyelination and axonal damage are not directly initiated by M. leprae but by infected macrophages that patrol axons; demyelination occurs in areas of intimate contact. PGL-1 confers this neurotoxic response on macrophages: macrophages infected with M. marinum-expressing PGL-1 also damage axons. PGL-1 induces nitric oxide synthase in infected macrophages, and the resultant increase in reactive nitrogen species damages axons by injuring their mitochondria and inducing demyelination. Our findings implicate the response of innate macrophages to M. leprae PGL-1 in initiating nerve damage in leprosy.
journal_name
Celljournal_title
Cellauthors
Madigan CA,Cambier CJ,Kelly-Scumpia KM,Scumpia PO,Cheng TY,Zailaa J,Bloom BR,Moody DB,Smale ST,Sagasti A,Modlin RL,Ramakrishnan Ldoi
10.1016/j.cell.2017.07.030subject
Has Abstractpub_date
2017-08-24 00:00:00pages
973-985.e10issue
5eissn
0092-8674issn
1097-4172pii
S0092-8674(17)30866-8journal_volume
170pub_type
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