Leprosy leads to “auto amputation,” or losing limbs due to injuries that go unnoticed due to lack of feeling, as well as skin lesions and other deformations. It can also cause blindness. Leper colonies to sequester those who might infect others are still operating around the world today, including Hawaii.
The scientists, funded by the National Institutes of Health, the Wellcome Trust, and the AP Giannini Foundation, studied leprosy in translucent young zebrafish, a tropical minnow that was a good test subject because, while the bacteria grow on mice footpads, they don’t cause nerve damage in the rodents.
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By genetically engineering parts of the fish’s nerves to be fluorescent green and dyeing the bacteria different fluorescent colors, too, they observed that the fish’s immune cells, or macrophages, consumed the bacteria but did not destroy it. They then attacked the myelin, or the protective insulations around the nerves. Alone, the leprosy bacteria didn’t hurt the nerves, however.
“We could watch everything live,” said Ramakrishnan. “We weren’t just taking snapshots. We could watch the macrophages crawl on the myelin and settle somewhere and see that the myelin was bubbling up only where the macrophages has settled. It was really the power of visualizing the sequence of events that turned out to unravel the secret.”
They discovered that a molecule identified as PGL-1 in leprosy, which is related to a similar compound in tuberculosis, caused the macrophages to overproduce nitric oxide that damaged cell mitochondria, or the cellular powerhouses that convert nutrition to energy.
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The researchers’ findings could help scientists around the world trying to wipe out a range of diseases, said Ramakrishnan.
“It’s very possible the lessons we learn now studying leprosy and its new recognition as an inflammatory disease is going to inform the mechanics, and possibility the treatment, of other neuro-inflammatory diseases,” said Ramakrishnan. “There could be a much wider swath.”
WATCH: What Happens When You Get Leprosy?