Eric Ghigo, INSERM
We’re studying a worm, the Planairium, or flatworm, it’s an invertebrate. We became interested in this worm because it has a strong survival capacity – it’s an immortal worm. You can cut it into little pieces and it regenerates. So we asked ourselves, if it has this high capacity to regenerate, does it also have any special immune responses, or ways to combat pathogens.
So we took the worm, fed it, infected it with disease carrying bacteria – 16 different bacteria that cause human disease including mycobacteria tuberculosis and we studied what it did with the bacteria. We noticed that, unlike humans or other organisms, it killed all the bacteria we tested, including mycobacteria tuberculosis. So we tried to understand the mechanism the worm used to resist these disease carrying bacteria, and to identify the mechanism in order to understand what happened in humans, and why humans aren’t able to fight bacteria such as mycobacterium tuberculosis.
We identified a series of genes that are involved in the worm’s resistance to the disease carrying bacteria. Among the genes we identified one, called « morn2 », that kills mycobacteria.
Then we looked at human white blood cells – to see if the same gene was there, because the worm can kill the bacteria, but humans can’. We saw that the gene is there, but it doesn’t work fully when it encounters the bacteria.
Then, we added the gene, in vitro, into human white cells and we saw that the human white cells developed the capacity to kill mycobacterium tuberculosis. This has opened a new direction for potential treatments against tuberculosis, to get rid of or more effectively fight this bacteria that affects humans.
Optimistically it might be in 10 years, first we have to go from the Planaria worm to cell cultures – we’ve started, we know how to do it – next we have to go to a much bigger model, maybe mice or even rabbits, maybe primates and finally we’ll get to humans.