The nerve damage, a hallmark of leprosy previously thought to be a byproduct of the immune systems response to the leprosy bacteria, now seems to be a direct result of the leprosy bug attaching itself to specialized nerve cells called Schwann cells, the glial, or supporting, cells of the peripheral nervous system (PNS).
The findings suggest that the bodys immune response does not play a significant role in the early stage of neurological injury.
The damage is characterized by the disruption of the myelin sheath, the insulation on nerve cell connections that helps transmit rapid signals between the brain and the peripheral organs, for example, skin and muscles. Damage to myelin causes loss of sensation, disability and paralysis.
Using laboratory cell tissue cultures and mice genetically manipulated to lack two key immune system cells, the research team, led by Rockefeller University microbiologist/cell biologist Anura Rambukkana, Ph.D., showed that Mycobacterium leprae (M. leprae), the bacterium that causes leprosy, destroys the protective myelin sheath that surrounds nerve fibers and then hides out in the supporting cells that enclose non-myelin nerve fibers, poised to initiate later attacks.
"What we show here is a novel mechanism of inducing demyelination by a bacterial pathogen," says Rambukkana. "This may unravel clues for early molecular events of neurodegeneration processes in other diseases, such as multiple sclerosis, which we currently know littleabout."
"By using this bacteria we will be able to obtain novel insight not only into the mechanism of the early demyelination process, but also how the complex molecular architecture of the demyelinated fiber is disr