Leprosy Bug Strips Nerves' Fatty Insulation

Researchers have long believed that the nerve damage that is a hallmark of leprosy, or Hansen’s disease, was caused by the immune system’s response to the bacterium Mycobacterium leprae. But a new study by James Salzer, M.D., Ph.D., Professor of Cell Biology and Neurology, and microbiologist Anura Rambukkana of Rockefeller University, shows for the first time that this notorious bacterium can directly harm nerve cells without involving the immune system.

	Schwann cells produce the fatty insulation called myelin that surrounds some nerve fibers

In the study, published in Science, Dr. Salzer and Dr. Rambukkana report that the bacterium strips away myelin, a fatty insulation that surrounds nerve fibers. Myelin is produced by Schwann cells, specialized supporting cells of the peripheral nervous system, and is critical for normal transmission of signals between the brain and the skin, muscles, and internal organs. The researchers also found unexpectedly that M.leprae did not have to enter the Schwann cells to cause degeneration of myelin.

Damage to the myelin sheath leads to loss of sensation and even paralysis. These devastating symptoms occur in such disorders as multiple sclerosis, leprosy, Guillain-Barré syndrome, and as a complication of diabetes. Little is known about what actually causes the loss of myelin.

We want to understand the events that lead to loss of myelin,” said Dr. Salzer. “These same signaling pathways may also be involved in the demyelination that occurs in the central nervous system. If we could find a way to manipulate these pathways, perhaps we could prevent the loss of myelin that occurs in various acquired and genetic disorders.”

The researchers used a “co-culture”system that Dr. Salzer helped establish years ago. In this system, Schwann cells from animals are placed in tissue culture and develop myelin. Twenty-four hours after attaching to the nerves, the leprosy bacterium produced significant damage to the myelin sheaths. Subsequently, the researchers used the bacterium to infect mice that had been genetically engineered to lack an immune system, and later found damage to myelin. They also discovered that the bacterium hides in certain cells that lack myelin, where it waits to initiate further attacks.